Evolution

Evolution
— Alpha and omega

A. No “Laws” of Evolution
The Night Sky at the Dawn of the Solar System
“The night sky would have been filled with bright stars, several at least as bright as the full moon.”
~ “The Long-Lost Siblings of the Sun”, Scientific American, Nov. 2009
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Self-organization:
Complexity of life
“The haemoglobin of our blood is a typical protein molecule. It is built up from chains of smaller molecules,
amino acids, each containing a few dozen atoms arranged in a precise pattern. In the haemoglobin molecule
there are 574 amino acid molecules. These are arranged in four chains, which twist around each other to
form a globular three-dimensional structure of bewildering complexity. A model of a haemoglobin molecule
looks rather like a dense thorn bush. But unlike a real thorn bush it is not a haphazard approximate pattern
but a definite invariant structure, identically repeated, with not a twig nor a twist out of place, over six
thousand million million million times in an average human body. The precise thorn bush shape of a protein
molecule such as haemoglobin is stable in the sense that two chains consisting of the same sequences of
amino acids will tend, like two springs, to come to rest in exactly the same three-dimensional coiled pattern.
Haemoglobin thorn bushes are springing into their ‘preferred’ shape in your body at a rate of about four
hundred million million per second, and others are being destroyed at the same rate.”
~ Richard Dawkins, The Selfish Gene (Oxford University Pres, 1976)
Haemoglobin molecule (Molecular Station)
“Let us define complexity as the difference between a maximally disordered state, i.e., a maximum entropy,
and the actual entropy with respect to the local environment (a thermodynamicist called Peter Landsberg
actually proposed this definition). Natural selection favours organisms that minimize entropy with respect to
environment. Those that don’t, die out. Therefore, mutations will eventually lead to lower local entropy
which, given that we subtract form the maximal total entropy to get complexity results in increased
complexity of life.”
“Given that we stated that life may maximize total entropy production this may imply that it also maximizes
complexity increase.”
~ Vlatdo Vedral, Decoding Reality (Oxford University Press, 2010), p. 89
Complex systems that self-organize and form a cell structure (such as flocks of birds or bubbles on a
boiling surface):
• Form spontaneously
• Oscillate
• Resist change in the overall pattern.
“…On many levels, the DNA code seems less a blueprint than an exquisite feedback relay center balancing
the negative feedback ability to maintain stability with the positive feedback ability to amplify change. An
inhabitant of the edge between order and chaos, DNA feedback is coupled with other feedback inside and
outside the individual organism — an instance of the cooperative, coevolutionary process that sustains and
transforms the life on the planet.”
~ John Briggs and F. David Peat, Turbulent Mirror (Harper and Row, 1990), p. 161
Simplified DNA Transcription/Translation Process
“Inside the cell there are four different components that enable it to self replicate:
i. the protein synthesizer machine, M,
ii. the biological non-engine (akin to the Xerox copier), X,
iii. enzymes which act as controllers switching the nano-engine on and off, C, and
iv. the DNA information set, I.” (p. 48)
“A group of three bases, such as ATC, is each associated with one amino acid. So given that there are four
bases, A, C, T, and G, we have … [43] 64 possible three-base-long combinations — and hence the
possibility of encoding 64 distinct amino acids. However, rather surprisingly, there are only 20 amino acids
in total…. meaning that … there is more than one triplet associated with the same amino acid. So, for
example, in Nature, ATT, ATC, ATG all encode the amino acid isoleucine, while AGA and AGG both
encode arginine.” (p. 49)
“There is a huge redundancy in how bases are combined to form amino acid chains. This is a form of error
correction.” (p. 56)
“Schrödinger was the first to argue convincingly that life maintains itself on low entropy through increasing
the entropy of its environment.” (p. 68)
“Since history is littered with environmental changes of some degree or another, it is clear that any DNA
that propagates will only ever get more complex (as it contains more and more information about
environmental changes)…. As a general theme … meaningful information necessarily emerges only as an
interplay between random events and deterministic selection. Each on its own is insufficient.” (p. 53)
“The central calculation that the DNA performs is matching base pairs and each of these matches costs
approximately a hundred units of energy. To re-create a whole new strand of DNA then requires around
one billion units of energy.” (p. 75)
“The increasing complexity of life is driven by the overall increase in disorder in the Universe.” (p. 77)
~ Vlatdo Vedral, Decoding Reality (Oxford University Press, 2010)
Metabolism first
“Nobel Laureate Christian de Duve has called for ‘a rejection of improbabilities so incommensurably high
that they can only be called miracles, phenomena that fall outside the scope of scientific inquiry.’ DNA,
RNA, proteins and other elaborate large molecules must then be set aside as participants in the origin of life.
Inanimate nature provides us with a variety of mixtures of small molecules, whose behavior is governed by
scientific laws, rather than by human intervention.
“Fortunately, an alternative group of theories that can employ these materials has existed for decades. The
theories employ a thermodynamic rather than a genetic definition of life, under a scheme put forth by Carl
Sagan in the Encyclopedia Britannica: A localized region which increases in order (decreases in entropy)
through cycles driven by an energy flow would be considered alive….Here I will try to list five common
requirements (and add some ideas of my own).
1) ”A boundary is needed to separate life from non-life.”

2) ”An energy source is needed to drive the organization process.”
3) ”A coupling mechanism must link the release of energy to the organization process that produces
and sustains life.”
4) ”A chemical network must be formed, to permit adaptation and evolution.”
5) ”The network must grow and reproduce.”
“Systems of the type I have described usually have been classified under the heading ‘metabolism first,’
which implies that they do not contain a mechanism for heredity. In other words, they contain no obvious
molecule or structure that allows the information stored in them (their heredity) to be duplicated and passed
on to their descendants. However a collection of small items holds the same information as a list that
describes the items. For example, my wife gives me a shopping list for the supermarket; the collection of
grocery items that I return with contains the same information as the list. Doron Lancet has given the name
‘compositional genome’ to heredity stored in small molecules, rather than a list such as DNA or RNA.
“The small molecule approach to the origin of life makes several demands upon nature (a compartment, an
external energy supply, a driver reaction coupled to that supply, and the existence of a chemical network
that contains that reaction). These requirements are general in nature, however, and are immensely more
probable than the elaborate multi-step pathways needed to form a molecule that can function as a replicator.”
“The principal initial task is the identification of candidate driver reactions — small molecule
transformations (A to B in the example before) that are coupled to an abundant external energy source (such
as the oxidation of carbon monoxide or a mineral)….Many potential paths to life may exist, with the choice
dictated by the local environment.
“An understanding of the initial steps leading to life would not reveal the specific events that led to the
familiar DNA-RNA-protein-based organisms of today. However, because we know that evolution does not
anticipate future events, we can presume that nucleotides first appeared in metabolism to serve some other
purpose, perhaps as catalysts or as containers for the storage of chemical energy (the nucleotide ATP still
serves this function today). Some chance event or circumstance may have led to the connection of
nucleotides to form RNA. The most obvious function of RNA today is to serve as a structural element that
assists in the formation of bonds between amino acids in the synthesis of proteins. The first RNAs may
have served the same purpose, but without any preference for specific amino acids. Many further steps in
evolution would be needed to ‘invent’ the elaborate mechanisms for replication and specific protein
synthesis that we observe in life today.
“If the general small-molecule paradigm were confirmed, then our expectations of the place of life in the
universe would change. A highly implausible start for life, as in the RNA-first scenario, implies a universe
in which we are alone. In the words of the late Jacques Monod, ‘The universe was not pregnant with life
nor the biosphere with man. Our number came up in the Monte Carlo game.’ The small-molecule
alternative, however, is in harmony with the views of biologist Stuart Kauffman: ‘If this is all true, life is
vastly more probable than we have supposed. Not only are we at home in the universe, but we are far more
likely to share it with unknown companions.’”
~ Robert Shapiro, “A Simpler Origin for Life”, Scientific American, February 12, 2007
Increasing genetic phase space

“The entire fabric of life on Earth requires the maintaining of a profound and subtle organization, which
undoubtedly involves entropy being kept at a low level. In detail there is an immensely intricate and
interconnected structure, which has evolved in keeping with the fundamental biological principle of natural
selection and with many detailed matters of chemistry.”
~ Roger Penrose, Cycles of Time (The Bodley Head, 2010), p. 77
“…Ecologist R. Ulanowitz has introduced a … mathematical measure for work flows in ecosystems. The
measure is the total energy flow in an ecosystem times the diversity of that energy flow. He has show that
nature ecosystems maximize this measure, while it drops to lower values for perturbed ecosystems.”
~ Stuart A. Kaufmann, Reinventing the Sacred (Basic Books, 2008), p. 99
“A law known as ‘Dollo’s law’ states the irreversibility of biological evolution: evolution never repeats
itself. Darwin’s natural selection does not necessarily prescribe progress or regression, does not imply a
direction of evolution in time, it only states an environmental constraint. Indirectly, Dollo’s law does: it
prescribes a trend towards more and more complex, and more and more ordered, living structures. Dollo’s
law expresses the visible fact that reproduction, ontogeny and phylogeny are biological organizations
whose behavior is irreversible: both during growth and during evolution, entropy of biological information
constantly increases.
Unlike Prigogine, biologist Daniel Brooks and the philosopher E.O. Wiley “believe that biological systems
are inherently different from dissipative structures. Biological systems, unlike physical systems, owe their
order and organization to their genetic information, which is peculiar in that it is encoded and hereditary.
Dissipation in biological systems is not limited to energy but also involves information, because of the
genetic code, which is transmitted to subsequent generations. Organisms simply live and die, they don’t
evolve. What evolves is the historic sequence of organisms, which depends on genetic code. The genetic
code must therefore be put at the center of any theory of evolution.
“Unlike most theories of information, that use information to denote the degree to which external forces
create structure within a system, Brooks-Wiley’s information resides within the system and is material, it
has a physical interpretation. It resides in molecular structure as potential for specifying homeostatic and
ontogenetic processes. As the organism absorbs energy from the environment, this potential is actualized
and is ‘converted’ into structure.
“What they set out to prove (following Lotka’s original intuition and exploiting Layzer’s ideas) is that
evolution is a particular case of the second law of Thermodynamics, that Dollo’s law is the biological
manifestation of that second law. Biological order is simply a direct consequence of that law. The creation
of new species is made necessary by the second law and is a ‘sudden’ phenomenon similar to phase
changes in Physics. Phylogenetic branching is an inevitable increase in informational entropy.
“In this scenario, the interaction between species and the environment is not as important in moulding
evolution: natural selection mainly acts as a pruning factor.
“Over short time intervals, biological systems do behave like dissipative structures. But over longer time
intervals, they behave like expanding phase space systems (as proved by Layzer). Their relevant phase
space is genetic, an ever increasing genetic phase space.”
~ Piero Scaruffi, “The Physics of Life” (excerpts from Thinking About Thought), 1998-2001
“…The more profitable life becomes the less profitable its environment (as it increases proportionally in
entropy). As the environment increases in entropy, this makes it more and more difficult for life to
propagate.”
~ Vlatdo Vedral, Decoding Reality (Oxford University Press, 2010), p. 87
A casually anomalous process

From biology “we have learned that the transformation of the laws can be coeval [contemporary] with the
transformation of the phenomena.”
~ Roberto Unger, Perimeter Institute workshop on the Laws of Nature: Their Nature and Knowability, May
22, 2010
“In living cells, rather amazingly, among the proteins encode by genes are those very proteins that carry out
translation [of RNA to proteins]…. In short, in contemporary cells, the molecular mechanism by which
cells reproduce form a complex self-referential system that clearly is highly evolved.” (p. 46)
“Collective autocatalysis with kinetic control is an example where the integrated system constrains the
kinetic behaviours of its parts and organizes the kinetic behaviours of the chemicals of which it is made.
These constraints yielding organization of process are partially causal in what occurs. These constraints,
imposed by the system’s causal topology on the kinetics of its parts, are a case of ‘downward causation.’
Because these constraints are partially causal, the explanatory arrows do not point exclusively downward to
the parts but also point upwards to the organization of the whole.” (p. 58)
“In humans, it is estimated that about 2,500 regulating genes encode 2,500 different transcription factors
and cofactors These 2,500 genes and other signaling proteins regulate one another and the remaining
22,500 genes.” (p. 105)
~ Stuart A. Kaufmann, Reinventing the Sacred (Basic Books, 2008)
This map of subnetwork centered around the gene cyclooxygenase-1 (COX1 or PTGS1) involved in
synthesis of prostaglandins, which control smooth muscle activity in the body along with many other
physiological functions. (Credit: UCLA)
~ “Scientists Map All Mammalian Gene Interactions”, ScienceDaily, Aug. 9, 2010
Ilya “Shmulevich found that for ordered and chaotic networks, as the number of model genes, N, increases,
the entropy increases for a while, then stops increasing! The behavior does not become more diverse as the
system size increases. In contrast, in critical networks, the entropy, or diversity of behaviours, continues to
increase as network size increases. Thus, only critical random Boolean networks can grow large and carry
out increasingly diverse, complex, coordinated behaviours.” (p. 117)
“…The evolution of the biosphere is radically nonpredictable and ceaselessly creative. If a scientific law is
(as the physicist Murray Gell-Mann concisely put it) a compact statement, available beforehand, of the
regularities of a process, then the evolution of the biosphere is partially beyond scientific law.” (p. 130)
“Let us call such situations causally anomalous…” (p. 134)

~ Stuart A. Kaufmann, Reinventing the Sacred (Basic Books, 2008)
“Chaitin is now applying incompleteness to evolution — something he calls ‘metabiology’. The idea stems
from his considerations of Turing’s work. The halting problem led Chaitin to formulate a number, known
as omega, that defines the probability of whether a randomly chosen program will halt or not in terms of a
string of 0s and 1s. Omega is infinitely long and irreducibly complex, and Chaitin has described it as the
DNA of mathematics. Now he is working out how to use omega to examine real DNA.
“If you think of DNA as a program for building and operating an organism, Chaitin says, you might be
able to discover the mathematics by which the information in DNA operates. Doing this, he says, may
show that evolution is the analogue of omega: infinitely complex and thus endlessly creative. ‘A way of
looking at Gödel and Turing’s work is that they were opening the door from pure mathematics to biology,’
Chaitin says.”
~ Michael Brooks, “The limits of knowledge: Things we’ll never understand”, New Scientist, 09 May 2011
Non-linear dynamics
“I suggest that the true source of macroevolutionary change lies in the non-linear, or chaotic, dynamics of
the relationship between genotype and phenotype — the actual organism and all its traits. The relationship is
non-linear because phenotype, or set of observable characteristics, is determined by a complex interplay
between an organism’s genes — tens of thousands of them, all influencing one another’s behaviour — and
its environment.
“Not only is the relationship non-linear, it also changes all the time. Mutations occur continually, without
external influence, and can be passed on to the next generation. A change of a single base of an organism’s
DNA might have no consequence, because that section of DNA still codes for the same amino acid.
Alternatively, it might cause a significant change in the offspring’s physiology or morphology, or it might
even be fatal. In other words, a single small change can have far-reaching and unpredictable effects — the
hallmark of a non-linear system.
“Iterating these unpredictable changes over hundreds or thousands of generations will inevitably lead to
evolutionary changes in addition to any that come about by the preferential survival of certain phenotypes. It
follows that macroevolution may, over the longer-term, be driven largely by internally generated genetic
change, not adaptation to a changing environment.
“The evolution of life has many characteristics that are typical of non-linear systems.
1. ”It is deterministic: changes in one part of the system, such as the mutation of a DNA base, directly
cause other changes. However, the change is unpredictable. Just like the weather, changes are
inexorable but can only be followed with the benefit of hindsight.
2. ”Behaviour of the system is sensitive to initial conditions. We see this in responses to glaciations in
the Quaternary period. The exact circumstances of the beginning of each interglacial determine the
development of the whole period, leading to unpredictable differences between interglacials
(Quaternary Science Reviews, vol. 14, p 967).
3. ”The history of life is fractal. Take away the labelling from any portion of the tree of life and we
cannot tell at which scale [i.e., class, order or species] we are looking. This self-similarity also
indicates that evolutionary change is a process of continual splitting of the branches of the tree.
4. ”We cannot rewind, as Stephen Jay Gould argued in Wonderful Life. Were we to turn the
evolutionary clock back to any point in the past, and let it run again, the outcome would be different.
As in weather systems, the initial conditions can never be specified to sufficient precision to prevent
divergence of subsequent trajectories.
“Life on Earth is always unique, changing, and unpredictable. Even if certain patterns can be dimly
discerned, our ability to do so diminishes with time, exactly as for the weather…. This view of life leads to
certain consequences. Macroevolution is not the simple accumulation of microevolutionary changes but has
its own processes and patterns. There can be no ‘laws’ of evolution. We may be able to reconstruct the
sequence of events leading to the evolution of any given species or group after the fact, but we will not be
able to generalise from these to other sequences of events.”
“In the last analysis, evolution can be likened to the description of human history as ‘just one damn thing
after another’, exactly as Fodor and Piattelli-Palmarini have argued.”
~ Keith Bennett, “The chaos theory of evolution”, New Scientist, 18 October 2010
(Also see “No finite description of evolutionary novelties”.)
“Autopoiesis and evolution, global stability and coherent change, appear in complementary manifestations
of dissipative self-organization. Whereas autopoiesis … may be described in terms of the complementary
part structure <−−> function, a three-fold correspondence holds for self-organization which includes
evolution:
structure ↔ function
[state, ma] [act, a]
⤡ ⤢
fluctuations
[relationship, et]
~ Eric Jantsch, The Self-organizing Universe, p. 44
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B. Development and Expression of the Genome
A Holobiontic Union:
A Lack of Genes
“Chromosomes can be divided into two types — autosomes, and sex chromosomes. Certain genetic traits
are linked to your sex, and are passed on through the sex chromosomes. The autosomes contain the rest of
the genetic hereditary information. All act in the same way during cell division. Human cells have 23 pairs
of large linear nuclear chromosomes, (22 pairs of autosomes and one pair of sex chromosomes) giving a
total of 46 per cell. In addition to these, human cells have many hundreds of copies of the mitochondrial
genome.”
~ Wikipedia
“One of the big shocks that emerged from the human genome project was that we have only around 23,500
genes — barely more than a nematode worm.”
“The coding parts of genes come in pieces, like beads on a string, and by splicing out different beads, or
exons, after RNA copies are made, a single gene can potentially code for tens of thousands of different
proteins, although the average is about five. Recent studies suggest up to 95 per cent of our genes may be
alternatively spliced in this way. Even more astonishingly, in at least one case in humans, RNA copies of
different genes are spliced together. If this is commonplace, it would vastly multiply the potential number of
different proteins.”
“Another recent discovery is that instead of having two copies of every gene — one from each parent —
we often have just one or three or more. This ‘copy number variation‘ is a result of big chunks of DNA
being lost or duplicated, and could help to explain much of the normal variation between individuals, as
well as diseases such as schizophrenia.”
~ Michael Le Page, “A dizzying journey into complexity”, New Scientist, 22 June 2010
(“How do cells read genetic information?”, Riken Research, 18 July 2008)
“When, in 2001, the human genome was sequenced for the first time, we were confronted by several
surprises. One was the sheer lack of genes: where we had anticipated perhaps 100,000 there were actually
as few as 20,000. A bigger surprise came from analysis of the genetic sequences, which revealed that these
genes made up a mere 1.5 per cent of the genome. This is dwarfed by DNA deriving from viruses, which
amounts to roughly 9 per cent.”
~ Frank Ryan, “I, virus: Why you’re only half human”, New Scientist, 29 January 2010
Retrotransposons
“…Huge chunks of the genome are made up of mysterious virus-like entities called retrotransposons,
pieces of selfish DNA that appear to serve no function other than to make copies of themselves. These
account for no less than 34 per cent of our genome.
“All in all, the virus-like components of the human genome amount to almost half of our DNA.”
Researchers at the University of Pennsylvania School of Medicine “determined that any two peoples’
genomes differ at roughly 285 sites out of the 1139 sites studied. These results were found by scanning the
genomes of 25 individuals, 15 of which were unrelated.”
“Retrotransposons are the major class of jumping genes, with the L1 family the most abundant type of
retrotransposon in the human genome. L1s comprise about 17 percent of the human genome and were the
subject of the Genome Research paper.”
“Eventually, continuous jumping by retrotransposons expands the size of the human genome and may
cause shuffling of genetic content. For example, when retrotransposons jump, they may take portions of
nearby gene sequences with them, inserting these where they land, and thereby allowing for the creation of
new genes. Even otherwise unremarkable insertions of L1s may cause significant effects on nearby genes,
such as lowering their expression.
“Retrotransposons move by having their DNA sequence transcribed or copied to RNA, and then instead of
the genetic code being translated directly into a protein sequence, the RNA is copied back to DNA by the
retrotransposon’s own enzyme called reverse transcriptase. This new DNA is then inserted back into the
genome. The process of copying is similar to that of retroviruses, such as HIV, leading scientists to
speculate that retroviruses were derived from retrotransposons.”
~ “Jumping Genes Provide Extensive ‘Raw Material’ for Evolution, Study Finds”, ScienceDaily, June 1,
2010
Endogenisation
Endogenize: “To develop something internally.” (Wiktionary)
“Endogenisation allows retroviruses to take genetic symbiosis to a new level. Usually it is an extension of
the normal infectious process, when a retrovirus infects a blood cell, such as a lymphocyte. But if the virus
happens to get incorporated in a chromosome in the host’s germ line (sperm or egg), it can become part of
the genome of future generations.”
“A virus integrating itself into the germ line brings not just its own genes, but also regulatory regions that
control those genes. Viral genomes are bookended by regions known as long terminal repeats (LTRs),
which contain an array of sequences capable of controlling not just viral genes but host ones as well. Many
LTRs contain attachment sites for host hormones, for example, which probably evolved to allow the virus
to manipulate host defences.”
“Such germ-line endogenisation has happened repeatedly in our own lineage — it is the source of all that
viral DNA in our genome. The human genome contains thousands of HERVs [human non-infectious
endogenous retroviruses] from between 30 and 50 different families, believed to be the legacy of epidemics
throughout our evolutionary history. We might pause to consider that we are the descendants of the
survivors of a harrowing, if brutally creative, series of viral epidemics.”
“Retroviruses will often endogenise repeatedly throughout the host genome, leading to a gradual
accumulation of anything up to 1000 ERVs. Each integration offers the potential of symbiogenetic
evolution.”
Regulatory sequences of HERVs include:

• construction and functioning of the human placenta
• embryonic development
• normal brain function
• gene regulation
“…The human genome has evolved as a holobiontic union of vertebrate and virus.”
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Endogenous Constraints:
Genetic ‘Rescue’
A large family of proteins called kinases “switch other proteins on or off by attaching a large negatively
charged phosphate group on them, a process that changes their shape and hence their catalytic activity…. In
the run-up to cell division, The cdc2 [cell division control] protein kinase switches on many proteins
required for the act.”
“Although the detailed mechanism of the cell clock remains mysterious, it is clear that the generic program
governing cell division has not substantially changed during the millions of years that life has existed on
Earth: yeasts and humans share a common ancestor that lived on Earth 1000 million years ago and used the
same control of cell division as we do today…”
~ Peter Coveney & Roger Highfield, The Arrow of Time: A Voyage Through Science to Solve Time’s
Greatest Mystery (W.H. Allen, 1990), p. 229
“Because highly conserved master genes can persist through hundreds of millions of years of evolution, it
is possible to perform experiments that exhibit aspects of genetic ‘rescue’. This means that a ‘healthy’
variant of a given gene, if suitably inserted into the embryo at a very early stage and then activated, can
successfully compensate for a ‘defective’ variant of that same gene (rescuing the function of the gene). This
is an impressive biotechnological feat, but it stands to reason that it works. What’s truly extraordinary is
that such genetic rescue can also accrue in organisms across distant species, illustrating both the extreme
complexity of genotype to phenotype relations and the reality of the conservation of genes over
evolutionary time.”
~ Jerry Fodor and Massimo Piattelli-Palmarini, What Darwin Got Wrong (2010), p. 28
“Genome biologists at New York University’s Center for Genomic and Systems Biology and Princeton
University’s Lewis-Sigler Institute for Integrative Genomics…. revealed significant differences in the range
of variation due to natural selection — those traits that are vital to the health of the organism, such as the
activity of genes required for the embryo to develop, were much less likely to vary than were those of less
significance to its survival, such as the activity of genes required to smell specific odors.”
~ “Gene’s Location on Chromosome Plays Big Role in Shaping How an Organism’s Traits Evolve”,
ScienceDaily, Oct. 14, 2010
Positions of genes
“One of first things biologists noticed was that genes reside in different parts of the nucleus depending on
their activity. Chromosomal regions containing silent genes localize to condensed DNA regions in the outer
periphery, whereas active genes stay in the roomier nuclear center, perhaps because there they can more
easily share the transcription resources. “
“Changes to nuclear structure can affect cellular function in dramatic ways. In April biologists Thomas
Cremer and Boris Joffe of the Ludwig-Maximilians University in Munich noticed that the architecture of
retina rod nuclei is inverted in nocturnal mice — condensed DNA sits at the center, with less condensed
regions in the periphery…. The researchers compared the retinal nuclei of 38 species and found that those
of nocturnal and crepuscular species — animals active at dusk or dawn — featured the inverted structure,
whereas diurnal species had the more traditional layout. The inverted architecture seems to minimize light
scattering, which allows them to see better in the dark, Joffe says, but it is unclear why.”
“Aging and disease are also associated with changes to nuclear architecture. Generally, as cells age, stores
of condensed DNA at the nuclear periphery start migrating inward.”
~ Melinda Wenner, “Positions of Genes Inside the Cell Nucleus Exert Biological Effects”, Scientific
American, October 2009
“Genome biologists at New York University’s Center for Genomic and Systems Biology and Princeton
University’s Lewis-Sigler Institute for Integrative Genomics…. found that genes located in the middle of a
chromosome were less likely to contribute to genetic variation of traits than were genes found at the ends.
In other words, a gene’s location on a chromosome influenced the range of physical differences among
different traits.”
“Using a mathematical model, they were able to show that genes located near lots of other genes are
evolutionarily tied to their genomic neighbors. Specifically, natural selection, in which variation among vital
genes is eliminated, also removes the differences in neighboring genes, regardless of their significance.”
~ “Gene’s Location on Chromosome Plays Big Role in Shaping How an Organism’s Traits Evolve”,
ScienceDaily, Oct. 14, 2010
Self-organizing chromosomes
Gene Activation
“Chromosomes are not sprinkled randomly around the inside of the nucleus. They occupy preferred
positions.”
“When researchers removed active genes from their regular location in the nuclear interior and tethered them
to the membrane that surrounds the nucleus, their activity was generally reduced. So the nuclear periphery
helps to keep at least some genes quiet.
“The nuclear interior, for its part, might also offer something special to chromosomes and genes whose
activity is required quickly or often: collections of protein conglomerates known as transcription factories.
These ‘factories’ are aggregations of the cellular components required to activate genes, including
polymerase enzymes (which transcribe DNA into RNA that is later translated into an encoded protein), as
well as transcription factors (proteins that bind to regulatory areas of genes and start the polymerases on
their way).
“When embryonic stem cells receive a signal to differentiate into, say, bone cells or neurons, their nuclear
architecture changes dramatically. Lamin proteins appear and join together to form a tight, interwoven mat
— the nuclear lamina — that sits under the nuclear membrane. This supportive lamina is believed to
maintain nuclear shape and to protect the chromosomes from external mechanical pressure. But it also
appears to be involved in normal gene regulation. Chromosome segments that have fewer active genes
contain a particular structural protein that compresses those regions into heterochromatin — and ties them to
the lamin proteins in the outskirts of the nucleus. That sequestration leaves the gene-rich areas closer to the
interior and to the gene factories that allow them to be active. Thus, the appearance of lamins during
embryonic development allows cells to shut down genes that are no longer needed, by banishing them to
the sidelines.”
“I have proposed that nuclear positioning is self-organizing…. Before the signal reaches the cell, the gene is
inactive — most likely tucked away in a section of condensed chromatin, perhaps even in a block of
heterochromatin hugging the nuclear periphery. When the signal arrives in the nucleus, molecules known as
chromatin remodeling complexes unfold the condensed DNA in and around the gene and make the region
more accessible to the transcriptional machinery. In a self-organizing nucleus, this relaxation would allow
that stretch of chromatin to loop out from the heterochromatin in the periphery and to flop around, exploring
new parts of the nucleus. With any luck, the meandering loop will eventually make contact with a
transcription factory.
“Note that this movement of the gene — from the nuclear outskirts to the center of the action — occurs
without the help of a dedicated transport machinery and is entirely driven by the activity of the gene itself.
Thus, the position of the gene is self-determined. This model has an intriguing consequence: it suggests that
although a gene’s nuclear location is not random, how it gets there can be.
“The self-organization concept agrees with many results from gene-tracking experiments. Genes can loop
out from chromosomes and travel through the nucleus. A few genes even take this transcriptional ticket-to-
wander to an extreme. When white blood cells are stimulated by hormones called cytokines, genes that
encode immune system proteins known as MHC class II molecules stray far away from the body of the
chromosome on which they are located — sometimes stretching halfway across the nucleus.
“The same principle may govern the positioning of entire chromosomes. Although most genes are rather
subtle in their movement, each makes a small contribution to where its chromosome will wind up in the cell.
So if self-organization is the rule, one would expect a chromosome that contains mostly inactive genes will
find itself pulled toward the more repressive regions in the nuclear periphery, whereas a chromosome
having predominantly active genes will be dragged toward the nuclear interior.
“To test this prediction, Mark Groudine and his colleagues at the Fred Hutchinson Cancer Center in Seattle
collected blood precursor cells and then triggered their maturation. At different points, cells were harvested,
and the activities of several thousand genes were measured. At the same time, the investigators monitored
the position of the chromosomes on which these genes were located. The results: the chromosomes that
harbored the largest number of genes whose activity changed as the cells matured showed the most
movement.”
~ Tom Misteli, “The Inner Life of the Genome”, Scientific American, February 2011
.....................................................................................................................
The Evolution of Biological Complexity:
Non-adaptive mechanisms
“Michael Lynch, an evolutionary theorist at Indiana University, teamed up with Ariel Fernandez of the
University of Chicago, both in the US, to look specifically at protein structure. They considered 106
proteins shared among 36 modern-day organisms of widely varying complexity, from single-celled
protozoa up to humans.
“The pair were studying ‘dehydrons’ — regions of proteins that make them more unstable in watery
environments. These dehydrons — first discovered by Dr Fernandez — make the proteins more sticky in
water, thereby raising the probability that they will adhere to other such proteins.”
~ Jason Palmer, “Protein flaws responsible for complex life, study says”, BBC News, 19 May 2011
Their paper, “Non-adaptive origins of interactome complexity”, Nature, 2011, “suggests that the random
introduction of errors into proteins, rather than traditional natural selection, may have boosted the evolution
of biological complexity. Flaws in the ‘packing’ of proteins that make them more unstable in water could
have promoted protein interactions and intracellular teamwork, expanding the possibilities of life.”
According to Fernández, “What we are claiming here is that inefficient selection creates a niche or an
opportunity to evolve complexity.”
“When mildly negative mutations arise in a species with a large population, such as the trillions of bacterial
organisms that can fill a small area, they are quickly cleared out by selective forces. But when a new
mutation appears in a species with a relatively small population, as in large mammals and humans, selection
against the error is slower and less efficient, allowing the mutation to spread through the population.
“A computational analysis of 106 orthologous [separated by a speciation event] proteins confirmed their
hypothesis that proteins from species with smaller populations were more vulnerable in water. The result
suggests that structural errors accumulate in large organisms such as humans due to random genetic drift.”
“On their own, these unstable proteins might be expected to perform their cellular duties more poorly,
possibly causing harm to the organism. But unstable proteins are also ‘stickier,’ more likely to form
associations with other proteins that could introduce more flexibility and complexity into the cell. If these
complexes create a survival advantage for the organism, forces of natural selection should take over and
spread the new protein complex through the population.”
~ “Errors in Protein Structure Sparked Evolution of Biological Complexity”, ScienceDaily, May 21, 2011
“These slight defects may decrease protein function even as they increase protein cooperation. The authors
suggest then that other adaptations occur that ‘undo’ the deleterious effects of the sticky proteins.
“For example, the protein haemoglobin that carries oxygen in our blood, is made of four identical subunits,
each with a range of dehydron flaws; simpler organisms have globin molecules that accomplish the same
job with just one subunit. But the overlap of the four subunits actually masks the flaws in each one.”
The haemoglobin protein in our blood contains four identical subunits co-operating
According to Ford Doolittle of Dalhousie University, “We tend to marvel at the Darwinian perfection of
organisms now, saying ‘this must have been highly selected for, it’s a tuned and sophisticated machine’. In
fact, it’s a mess — there’s so much unnecessary complexity.”
~ Jason Palmer, “Protein flaws responsible for complex life, study says”, BBC News, 19 May 2011
“The implication that complexity initially arose by accident may be provocative within the field of
evolutionary biology, the authors said. The discovery that flawed proteins are more likely to form
complexes could also revolutionize the growing field of bioengineering, where the tools of evolution are
used to create stronger, self-assembling, or self-repairing materials.”
Fernández says, “Natural designs are often one notch more sophisticated than the best engineering. This is
another example: Nature doesn’t change the molecular machinery, but somehow it tinkers with it in subtle
ways through the wrapping.”
~ “Errors in Protein Structure Sparked Evolution of Biological Complexity”, ScienceDaily, May 21, 2011
Molecular Drive
“Variation on the order of thousands to hundreds of thousands of DNA’s smallest pieces [SNPs — single
nucleotide polymorphisms] — large swaths varying in length or location or even showing up in reverse
order — appeared 4,205 times in a comparison of DNA from just four people, according to a study
published May 31 in the Proceedings of the National Academy of Sciences.”
~ “Powerful Genome Barcoding System Reveals Large-Scale Variation in Human DNA”, ScienceDaily,
June 1, 2010
Gabriel Dover “stresses that all genomes of all examined species from bug to worms to humans are riddled
with the ubiquitous genomic mechanism of turnover (replicative transposition, inversion, duplication) that
power what he calls molecular drive. The recurrent instability of genomes leads to reorganizations and to
new temporary stabilizations. Dover stresses that the spreading consequences of molecular drive also work
in exactly the same way (sampling error) that stochastic genetic drift works at the phenotype level. Besides
gene conversion (biased and unbiased) … there are transpositions, slippages unequal crossing over of
chromosomes and other processes, which together endure, in Dover’s picture, that what starts off as a
single mutation in a single gene in a single chromosome in a single individual can, with the passing of the
generations, spread throughout a sexually reproducing population. This internally driven spreading process
can open up, for a population, in the course of time, paths of development and reproduction and behaviour
that were previously inaccessible to it.”
~ Jerry Fodor and Massimo Piattelli-Palmarini, What Darwin Got Wrong (2010), pp. 37-38
“We wanted to know if the divergent evolution between proteins was still proceeding. Today, we can find
proteins that are still similar after almost 3.5 billion years of evolution. Our study showed that their
divergence continues with these proteins becoming more and more different despite their incredible level of
conservation,” said Fyodor Kondrashov, principal investigator of the project and leader of the Evolutionary
Genomics group at the CRG.
~ “Big Bang in the Protein Universe?”, ScienceDaily, May 21, 2010
The complexity of a single gene

Joseph H. Nadeau, director of scientific development at the Institute for Systems Biology in Seattle, “has
experimental evidence that the function of one particular gene sometimes depends on the specific
constellation of genetic variants surrounding it — an ensemble effect that introduces a contextual,
postmodern wrinkle to genetic explanations of disease. It suggests, Nadeau says, that some common
illnesses may ultimately be traceable to a very large number of genes in a network or pathway whose effects
may each vary depending on the gene variants a person has; the presence of one gene variant, way, can
exacerbate or counteract the effect of another disease-related gene in the group. ‘My guess is that this
unconventional kind of inheritance is going to be more common that we would have expected,’ Nadeau
says.”
~ Stephen S. Hall, “Revolution Postponed”, Scientific American, October 2010
“…The segments of a gene that actually encode segments of proteins (these are called exons, while the
segments that do not code for proteins are called introns) can be spliced in different alternative ways. As a
result, a single gene can code for many different proteins, and a single mutation in one of the axons can
affect many of these proteins in a single stroke…. Over 90 percent of human genes [totalling 24,000] are
now estimated to undergo alternative splicing, exploiting this form of mRNA processing the yields multiple
proteins from a single gene.”
~ Jerry Fodor and Massimo Piattelli-Palmarini, What Darwin Got Wrong (2010), pp. 36-37
An RNA Machine
“…We suggest that the mammalian genome, rather than being viewed as islands of protein-coding
sequences in a sea of evolutionary junk, may be more accurately thought of as an RNA machine wherein
most information is expressed as non-coding (nc)RNAs in a developmentally regulated manner to
orchestrate the precise patterns of gene expression during mammalian ontogeny.”
~ P.P. Amara and J.S. Mattick, “Noncoding RNA in Development”, Mammalian Gnome, Vol. 19, 2008
“In the new model of biology, proteins still do the hard work of catalyzing reactions and switching genes
on and off, but the microRNAs regulate the amount of proteins and hence how much of each specific job is
done. At a minimum, the result is an incredibly complex web of cellular signals that are constantly working
together (or in opposition, as the case may be) to adjust the number and type of proteins expressed in a cell
and so, ultimately, the health of the cell itself. The ubiquitous cloud of microRNA regulation amounts to a
forward-looking feedback system. Every time a gene is switched on and sets about being transcribed to
make a protein, it might also generate one or more microRNAs that would, in turn, trigger a spectrum of
simultaneous adjustments or changes throughout the cell.”
~ Gary Taubes, Discover, “The Sea Change That’s Challenging Biology’s Central Dogma”, October 2009
“Early studies suggested that gene activity was regulated mainly by transcription factors — proteins that
bind to DNA, blocking or boosting the production of RNA copies of a gene and thus the amount of protein
that gene produces.
“While transcription factors do play a big role, cells also produce a wide variety of RNAs that, rather than
coding for a protein, control gene activity. Some, dubbed small interfering RNAs (siRNAs), form
complexes that seek out and destroy RNA copies of genes with a complementary sequence, preventing
protein production. MicroRNAs work in a similar way but are not as specific, controlling the activity of
many genes simultaneously. Piwi-acting RNAs, meanwhile, shut down the parasitic genes that litter our
genome to stop them wreaking havoc, though it’s not clear how.”
~ Michael Le Page, “A dizzying journey into complexity”, New Scientist, 22 June 2010
.....................................................................................................................
Evolvability:
Polygenic adaptation
“It turns out that the [human] genome actually contains few examples of very strong, rapid natural selection.
Instead most of the natural selection visible in the genome appears to have occurred over tens of thousands
of years. What seems to have happened in many cases is that a beneficial mutation spread through a
population long ago in response to a local environmental pressure and then was carried into faraway locales
as the population expanded into new territories. For example, some gene variants involved in determining
light skin color, an adaptation to reduced sunlight, are distributed according to ancient migration routes,
rather than just latitude. That these ancient selection signals have persisted over millennia without new
environmental pressures overwriting them indicates that natural selection of ten operates at a far more
leisurely pace than scientists had envisioned.”
“Overall the genomes of any two people are extremely similar, differing in only about one out of every
1,000 nucleotide pairs. Sites where one nucleotide pair substitutes for another are referred to as single
nucleotide polymorphisms, or SNPs (pronounced ‘snips’), and the alternative versions of the DNA at each
SNP are called alleles. Because most of the genome does not encode proteins or regulate genes, most SNPs
probably have no measurable effect on the individual. But if a SNP occurs in a region of the genome that
does have a coding or regulating function, it may affect the structure or function of a protein or where and
how much of the protein is made. In this way, SNPs can conceivably modify almost any trait, be it height,
eye color, ability to digest milk, or susceptibility to diseases such as diabetes, schizophrenia, malaria and
HIV.
“When natural selection strongly favors a particular allele, it becomes more common in the population with
each generation, while the disfavored allele becomes less common. Eventually, if the environment remains
stable, the beneficial allele will spread until everyone in the population carries it, at which point it has
become fixed in that group.”
“…If it usually has taken 50,000, not 5,000, years for a helpful allele to spread through a population, how
would humans ever manage to adapt quickly to new conditions? Although the best understood adaptations
arise from changes in a single gene, it may be that most adaptations do not arise that way but rather stem
from genetic variants having mild effects on hundreds or thousands of relevant genes from across the
genome — which is to say they are polygenic.”
~ Jonathan K. Pritchard, “How We Are Evolving”, Scientific American, October 2010
Evolutionary Capacitors
“Two factors are key [to evolvability]. Perhaps the most fundamental of these is an organism’s ‘mutational
robustness’ — the capacity to develop normally despite the presence of genetic mutations.”
“In fact, by neutralising the effects of otherwise harmful mutations, robustness preserves genetic variations
that might otherwise be weeded out. That means organisms accumulate a wealth of hidden mutations within
the population. Further genetic or environmental changes might then remove the buffering mechanisms and
unmask the effects of these stored mutations, providing ready-made variation in the organism’s make-up.”
“The main players seem to be ‘heat-shock proteins,’ according to studies led by Susan Lindquist at the
Massachusetts Institute of Technology. HSPs ensure that other proteins always fold in the same stable
three-dimensional shape, which is vital for their role within the cell. Under harsh conditions like scorching
temperatures or high salinity, proteins can fold wrongly, preventing them from carrying out their function.
It is here that the HSPs step in, acting as chaperones to guide the protein into the correct shape and allowing
it to function properly even under troublesome circumstances.
“Crucially, HSPs also ensure a protein folds into the same stable shape even in the face of genetic mutations
that shuffle the protein’s sequence of amino acids. That permits hidden variation to build up over time
without getting in the way of the protein’s everyday activities.”
~ Dan Jones, “Evolvability: How to cash in on the genetic lottery”, New Scientist, 01 July 2010
“A mutation in this protein [HSP90 ] generates all sorts of monstrosities in the fruit fly. … After several
artificial selections, some individuals carrying these anomalies are produced and the anomalous traits are
stably maintained, even after the HSP90 has been brought back, by genetic implants, to it normal state.
Geneticists … can conclude that proteins such as HSP90 act as ‘evolutionary capacitors. This means that
some potentially deleterious mutations can be kept at bay for generations passed on from one generation to
the next but remaining inert, until some other mutation, or major changes in the environment, can expose
them, that is can make of that genotype a corresponding phenotype.”
A nested hierarchy of modules

“The second key factor [to evolvability concerns a phenomenon known as integration — the way different
body parts or traits appear to vary and evolve together. Integration between traits often results from their
shared evolutionary history. Body parts like limbs, teeth, ribs and vertebrae that are repeated along the body
axis, for example, arose through the direct duplication of certain genes way back in evolutionary history.
The two copies will not be completely independent of one another because the expression of both will
ultimately be governed by the same regulatory genes at a different point in the genome, meaning the two
body parts would still tend to vary and evolve together.”
“The take-home message is that animals are made up of a ‘nested hierarchy’ of modules and integrated
traits, says Hallgrimsson [University of Calgary]. So while the bones of the arms and hands show reduced
integration in humans (and great apes generally) compared with quadrupedal monkeys, integration was
nonetheless strong enough between human hands and feet [big toe and thumb] to have profound
evolutionary consequences. It is these specific patterns of integration and modularity, rather than either
factor independently, that ultimately determines evolvability, he says.”
“About 540 million years ago, the Cambrian explosion led to the emergence of the basic body plans of the
35 or so phyla of animals recognised today. Their common ancestor had not achieved a high level of
integration or robustness, making it developmentally flexible and primed for evolutionary innovation.
Evolution cashed in on that flexibility but soon pushed for greater developmental integration, more or less
fixing the 35 body plans in the process.”
“Although the developmental processes that produce the basic body plans of animals are too tightly
integrated for fundamental change, a further drive towards greater modularity among parts of animals has
increased their individual evolvability. “
________________________________________________________________________
C. Inheritance of Acquired Changes
“…Lamarck’s very reasonable notion that fields (‘les fluides incontenables’ [fluids that can contain but
cannot themselves be contained’] played a fundamental role in evolution was eclipsed by Darwin’s
mathematical notion that the wonderful forms in nature are local, independently existing systems that arrive
‘mechanically’, by ‘random chance variation’. Allegedly, those random variants that ‘happened to fit well’
in the environment are the ones that proliferate and persist due to their superior ‘fitness’.”s
~ Ted Lumley, “Is Calculus Taking Science (And Us) On A Mad Joyride?”, Aboriginal Physics Newsletter
“Evolutionary-genomic studies show that natural selection is only one of the forces that shape genome
evolution and is not quantitatively dominant, whereas non-adaptive processes are much more prominent
than previously suspected.”
~ Eugene Koonin, Nucleic Acids Research (vol 37, p 1011), March 2009
.....................................................................................................................
Epigenetic Effects:
Genomic imprinting
“Inside a cell, genetic material takes the form of a complex package of DNA and histone proteins called
chromatin. It is modification of this structure — commonly by adding a methyl group in a process known
as methylation — that leads to epigenetic effects. Epigenetic effects can be induced by signals from within
the cell or from other cells. Exposure to nutritional, chemical or physical environmental factors such as food
shortage or temperature changes can result in lifelong changes for the organism. Sometimes epigenetic
effects are even passed on to the next generation, in which case the process is known as genomic
imprinting. It is this that provides another arena for sexual conflict — if one parent selectively switches off
or ‘silences’ genes coming from the other. Here females seem to win out.”
~ Pat Monaghan, “Who’s the Daddy”, New Scientist, 27 February 2010
a b
c
a) ”Enzymes attach chemical caps called methyl groups to cytosine, one of the four base units that
make up DNA.
b) ”Methyl and other groups can also be added to protein strands on histones, components of disc-
shaped proteins that serve as molecular cotton reels for DNA.
c) ”Methylation can pronto or decrease the activity of a gene so that genes throughout the body and
throughout life can be activated at different stages of development.”
~ Andy Coghlan, “Genes marked by stress make grandchildren mentally ill”, New Scientist, 03 November
2010
The RCC1 chromatin protein interacting with the nucleosome.

(Credit: Song Tan laboratory, Penn State University)
“The imprinted genes include several with a role in embryo growth and development, most of which are
also expressed in the brain, meaning that key traits like body size, cognitive ability and personality might be
moulded by epigenetic inheritance.”
“Genomic imprinting is rare because most of the methyl groups that have accumulated on DNA over an
individual’s lifetime are stripped away following fertilization. However, some do make it through to the
next generation — and a few years ago a team led by Toru Nakano at Osaka University in Japan,
discovered that mothers appear to manipulate this process. They found that demethylation mostly affects the
DNA that embryos inherit from the father, while the mother’s DNA is protected by a special protein in the
egg produced by a gene called stella (Nature Cell Biology, vol 9, p 64).”
~ Pat Monaghan, “Who’s the Daddy”, New Scientist, 27 February 2010
Research by Professor Ryszard Maleszka of The Australian National University’s College of Medicine,
Biology and Environment, and colleagues “reveals for the first time the intricacies of … DNA methylation
… This finding is not only crucial, but far reaching, because the enzymes that mark DNA in the bee are also
the enzymes that mark DNA in human brains,” said Professor Maleszka.
“In the bees, more than 550 genes are differentially marked between the brain of the queen and the brain of
the worker, which contributes to their profound divergence in behaviour. This study provides the first
documentation of extensive molecular differences that may allow honey bees to generate different
reproductive and behavioural outcomes as a result of differential feeding with royal jelly.”
According to Professor Maleszka, “This study represents a giant step towards answering one of the big
questions in the nature-nurture debate, because it shows how the outside world is linked to DNA via diet,
and how environmental inputs can transiently modify our genetic hardware.”
~ “Bees Reveal Nature-Nurture Secrets: Extensive Molecular Differences in Brains of Workers and
Queen”, ScienceDaily, Nov. 3, 2010
Early trauma
“The most compelling evidence for the epigenetic heritability of psychiatric illness comes from a recent
study of male mice made depressed by exposure to stress and lack of maternal care during the first two
weeks after birth. Isabelle Mansuy at the University of Zurich, Switzerland, and colleagues found that two
generations of offspring born to these mice were also depressed and anxious — even though they were
raised with the usual levels of maternal care and attention.
“…Mansuy’s team found that the relevant genes were over or under-methylated in the sperm of stressed
males and in the brains and germ lines, eggs or sperm of their offspring. ‘This provides proof that the
changes in DNA methylation are heritable,’ says Mansuy.”
“Recent studies by Margaret Morris and Jayanthi Maniam of the University of New South Wales in
Australia have shown that ‘comfort’ food and opportunities for exercise reversed epigenetic abnormalities
in rats caused by early-life stress (Psychoneuroendocrinology, DOI: 10.1016/j.psyneuen.2010.05.012).”
~ Andy Coghlan, “Genes marked by stress make grandchildren mentally ill”, New Scientist, 03 November
2010
“Low cortisol levels have been linked with PTSD, perhaps because people with this disorder are in a
prolonged state of stress. Sure enough, Yehuda [Rachel, who directs the Traumatic Stress Studies Division
of the Mount Sinai School of Medicine in New York City] showed that her group of Holocaust survivors
with PTSD had low cortisol. But she also discovered that their children had low cortisol levels too, and that
the more severe the parent’s symptoms, the lower the child’s cortisol was (Psychoneuroendocrinology,
vol. 27, p 171).”
In 2004, a group lead by Michael Meaney, a neuroscientist at McGill University “reported a fascinating
insight into the molecular mechanisms behind this effect. Cortisol winds down the stress response once a
threat has passed by binding to what are called glucocorticoid receptors in the brain, including in the
hippocampus. Meaney’s group showed that neglected rats had fewer glucocorticoid receptors in their
hippocampus, and that this was a result of epigenetic changes affecting the activity of the receptor’s gene. It
seemed as though the early maternal neglect had turned down the gene’s ‘volume control’ in the
hippocampus, meaning fewer receptors were made, resulting ultimately in an exaggerated stress response.”
“How well do those findings translate to humans? In 2009, Meaney’s group tried to answer that question
by studying brain taken from 24 people who had committed suicide … Those who had been abused had
fewer glucocorticoid receptors in their hippocampus than those without such a history — just like the
neglected rats (Nature Neuroscience, vol 12, p 342). And they had the same pattern of epigenetic changes
to the gene’s volume control in their hippocampus.”
Yehuda “studied a different group of survivors: women who had been at or near the World Trade Center in
New York City at the time of the September 2001 attacks, and who had been pregnant at the time. The
advantage in their case was that their babies’ cortisol levels could be tracked from an early age. Of the 38
women who were studied, about half had developed PTSD, and these had lower cortisol levels than the
rest. More significantly, so did their 9-month-old babies (Journal of Clinical Endocrinology and
Metabolism, vol. 90, p 4115).
“Jonathan Seckl, a hormone specialist at the University of Edinburgh, UK, who worked with Yehuda on
the 9/11 study, saw a research opportunity arising from the great popularity of licorice sweets in Finland.
The sweet aniseed taste of licorice comes from a compound called glycyrrhizin, which happens to block an
enzyme in the placenta that normally breaks down maternal cortisol and cuts the amount that reaches the
fetus. In theory, pregnant women who eat lots of licorice expose their babies to more cortisol.
“Seckl’s team found that the 8-year-old children of women who had eaten lots of licorice when pregnant —
equivalent to 500 milligrams of glycyrrhizin per week, or more — had 20 per cent more salivary cortisol on
waking than the children of mothers who ate the least. Alarmingly, it also affected their behaviour. The
children in the high-licorice group were more prone to breaking the rules, aggression and attention-deficit
hyperactivity disorder (American Journal of Epidemiology, vol. 170, p 1139).”
“Seckl and Meaney have found that in pregnant rats treated with glucocorticoids, the resulting metabolic
changes in their offspring also appear in the following generation, although not in the one after that. This
appears to be mirrored in people, according to a Swedish study showing a link between childhood nutrition
in the first generation studied, and disease risk in their grandchildren (European Journal of Human
Genetics, vol. 14, p 159). If those findings are borne out it would be radical indeed, as epigenetic signals
are supposed to be wiped clean in the cells that give rise to sperm and eggs (New Scientist, 6 November
2010, p 8).”
~ Laura Spinney, “Born scared: How your parents’ trauma marks your genes”, New Scientist, 24
November 2010
Built-in randomness generator

“…The inheritance of acquired changes could be seen as a source of variation that is then acted on by
natural selection — a view much closer to Darwin’s idea of pangenesis than Lamarck’s claim that the intent
of an animal could shape the bodies of its offspring. But even this idea is problematic, because it is very
rare for acquired changes to last longer than a generation (Annual Review of Genomics and Human
Genetics, vol. 9, p 233).”
“There is evidence that epigenetic changes, as opposed to genetic mutations or environmental factors, are
responsible for a lot of variation in the characteristics of organisms. The marbled crayfish, for instance,
shows a surprising variation in coloration, growth, lifespan, behaviour and other traits even when
genetically identical animals are reared in identical conditions. And a study last year found substantial
epigenetic differences between genetically identical human twins. On the basis of their findings, the
researchers speculated that random epigenetic variations are actually ‘much more important’ than
environmental factors when it comes to explaining the differences between twins (Nature Genetics, vol. 41,
p 240).”
According to Andrew Feinberg, a leading geneticist at Johns Hopkins University, “life has a kind of built-
in randomness generator which allows it to hedge its bets. For example, a characteristic such as piling on
the fat could be very successful when famine is frequent, but a drawback in times of plenty. If the good
times last for many generations, however, natural selection could eliminate the gene variant for piling on fat
from a population. Then, when famine does eventually come, the population could be wiped out.
“But if there is some uncertainty about the effect of genes, some individuals might still pile on the fat, even
though they have the same genes as everyone else. Such individuals might die young in good times, but if
famine strikes they might be the only ones to survive. In an uncertain world, uncertainty could be crucial for
the long-term survival of populations.”
“We already know there is a genetic lottery…. If Feinberg is right, there is also an epigenetic lottery: some
people are more (or less) likely to develop cancer, drop dead of a heart attack or suffer from mental health
problems than others with exactly the same DNA.”
Feinberg’s colleague Rafael Irizarry, a biostatistician at the Johns Hopkins Bloomberg School of Public
Health in Baltimore, produced “a list of genes associated with each region that could, in theory at least, be
affected by the variation in methylation. What he found blew him away. The genes that show a high degree
of epigenetic plasticity are very much those that regulate basic development and body plan formation. ‘It’s a
counter-intuitive and stunning thing because you would not expect there to be that kind of variation in these
very important patterning genes,’ says Feinberg.
“The results back the idea that epigenetic changes to DNA might blur the relationship between genotype (an
organism’s genetic make-up) and phenotype (its form and behaviour). ‘It could help explain why there is so
much variation in gene expression during development,’ says Günter Wagner, an evolutionary biologist at
Yale University. But that does not necessarily mean epigenetic changes are adaptive, he says. ‘There has
not been enough work on specifying the conditions under which this kind of mechanism might evolve.’”
~ Henry Nicholls, “Uncertainty principle: How evolution hedges its bets”, New Scientist, 10 January 2011
________________________________________________________________________
D. From Genotype to Phenotype
Evolution of Ontogenies:
Generating heritable phenotypes

Günter Wagner, a pioneer in the field who is based at Yale University, therefore defines evolvability as ‘the
capacity to generate heritable phenotypic variation’. That is to say, variation in an organism’s body-type that
can be passed from generation to generation.”
“Natural selection, the key mechanism of evolution, is only as good as the random mutations that arise. If a
given mutation is beneficial, it may propagate but the most beneficial mutations imaginable, alas, never
appear.”
~ Gary Marus, quoted in Future Babble (Clelland & Stewart Ltd., 2010)
“As a result, an evolutionary solution to an environmental problem that is flawed or sub-optimal but
nonetheless does the job — a kluge, in other words — may spread and become standard operating
equipment for the species. Once in place, the new equipment may be used to deal with other problems if,
once again it does the job adequately. And when new challenges arise, it may be the platform on which new
less-than-perfect solutions will be built — thus multiplying the quirks and oddities.”
~ Dan Garner, Future Babble (Clelland & Stewart Ltd., 2010), pp. 68-9
“A phenotype is any observable characteristic or trait of an organism: such as its morphology,

development, biochemical or physiological properties, behavior, and products of behavior (such as a bird’s
nest).”
~ Wikipedia
“It is naive to assume that there are independent genes for each and every characteristic that have
accumulated through past episodes of natural selection. The nature of biology is such that the basis of
individuality is largely uncapturable, making all talk of the evolutionary origins of the unknown premature
at best and vacuous at worst … Selection is not a process as such with predictable outcomes based on
fixed, selective ‘powers’ of individual genes controlling aspects of phenotype. Selection involves whole
phenotypes which are in part influenced by their unique combination of genetic interactions. Genetic
interaction are phenotypic, not genotypic. Advocacy of the gene as the unit of selection is operationally
incoherent and genetically misconceived.”
~ Gabriel Dover, 2006
“Darwinists say that evolution is explained by the selection of phenotypic traits by environmental filters.
But the effects of endogenous structure can wreak havoc with this theory. Consider the following case:
traits t1 and t2 are endogenously linked in such a way that if a creature has one, it has both. Now the core of
natural selection is the claim that phenotypic traits are selected for their adaptivity, that is, for their effect on
fitness. But it is perfectly possible that one of two linked traits is adaptive but the other isn’t; having one of
them affects fitness but having the other one doesn’t. So one is selected for and the other “free-rides” on
it…. Free-riding shows that the general claim that phenotypic traits are selected for their effects on fitness
isn’t true.”
“…When phenotypic traits are endogenously linked, there is no way that selection can distinguish among
them: selection for one selects the others, regardless of their effects on fitness.”
~ Jerry Fodor and Massimo Piattelli-Palmarini, “Survival of the fittest theory”, New Scientist, 3 February
2010
“…The classical model of neo-Darwinism represented the manifest (phenotypic) consequences of internal
changes in the genes (genotypic variants) as a unidimensional arrow from genotypes to phenotypes. In
essence, it abstracted from all effects of development on visible traits, aside from the effects of genetic
mutations, which were themselves considered to be largely independent of one another. But the internal
developmental filters that neo-Darwinism tried so hard to abstract from now increasingly seem to be at the
very core of evolution. Genes and phenotypes still count, of course; but the evo-devo revolution has
stressed that evolution is essentially the evolution of the arrow that connects them. The slogan is, evolution
is the evolution of ontogenies. In other words, the whole process of development, from the fertilized egg to
the adult, modulates the phenotypic effects of genotypic changes, and thus ‘filters’ the phenotypic options
that ecological variables ever have a chance to select from.”
Parallels between ontogeny and phylogeny
Ernst Haeckel’s famous comparative analysis of vertebrate development
“Whether fish or flies — at a certain stage in their development, the embryos of different animal species
within a phylum are almost impossible to distinguish on the basis of their appearance. The greatest
similarity arises in the middle of embryonic development, during the ‘phylotypic stage’; species-specific
differences predominate before and after this stage. This observation is illustrated by the hourglass model.”
“For the first time, scientists have now demonstrated that the hourglass motif arises in organisms as diverse
as the fruit fly and zebrafish, not only at morphological level but also at molecular level — a finding that
suggests that parallels do, indeed, exist between ontogeny and phylogeny. In a study carried out on six fruit
fly species (Drosophila sp.), the research group working with Pavel Tomancak at the Max Planck Institute
of Molecular Cell Biology and Genetics in Dresden discovered that the similarities not only in morphology,
but also in the expression pattern of the genes are greatest during the phylotypic stage; before and after this
phase, the differences between the species are greater. Moreover, the scientists also observed that the
expression pattern of key genes reflects the hourglass model most faithfully. Meanwhile, Tomislav
Domazet-Lošo and Diethard Tautz, researchers at the Max Planck Institute for Evolutionary Biology in
Plön, demonstrated with zebrafish (Danio rerio) that the phylogenetically oldest genes are active during the
phylotypic stage and that, before and after this stage, the most active genes are those that arose later in
evolutionary history. The Plön-based evolutionary biologists also made another astonishing discovery: they
observed that in adult zebrafish progressively older genes are also activated with the increasing age of the
animals. The same conclusion was reached in comparative analyses carried out on Drosphila , mosquitoes
of the genus Anopheles and threadworms.”
~ “Similarities in the Embryonic Development of Various Animal Species Are Also Found at Molecular
Level”, ScienceDaily, Dec. 15, 2010
.....................................................................................................................
Physiological Development:
Laws of Form
Complexity of form in rotolaria
“Neo-Darwinists are keen to say that natural selection never optimizes, it only finds locally satisfactory
solutions…. It is important to our critique of neo-Darwinism that the problem of finding optimal solutions
to evolutionary problems by filtering candidates generated at random wold often be intractable. But … there
are some instances of optimal (or near-optimal) solutions to problems in biology; so, if natural selection
cannot optimize, then something else must be involved. Very plausibly the ‘something else’ includes:
physics, chemistry, autocatalytic processes, dissipative strutters and principles of self-organization and
surely other factors that the progress of science will in due time reveal.”
Belousov-Zhabotinsky Reaction
“The ‘Belousov-Zhabotinsky reaction’ is a family of oscillating chemical reactions in which transition-metal

ions or complexes catalyze the oxidation of a substrate by bromate in acidic, aqueous solution. In a stirred
solution, nearly periodic oscillations occur in the concentrations of the oxidized and reduced forms of the
catalyst. In a thin, unstirred layer of the reaction mixture, one can observe patterns in time and space.”
~ Scholarpedia
“One of the most longstanding and challenging problems in biology appears to be solved: why metabolic
rate scales as the 3/4 power of body mass.
“The answer is that organisms effectively live in four spatial dimensions. They have exploited fractal
geometry so that critical linear dimensions and surface areas scale as the 1/4 and 3/4 powers of body mass,
respectively, rather than the 1/3 and 2/3 powers expected from conventional Euclidean geometry.”
1/3 Power
1/4 Power
2/3 Power
3/4 Power
“ We have developed a general model which is based on the assumption that biological rates and times are
ultimately limited by the rates at which limited energy and materials can be supplied to cells through a
hierarchical branching network. It further assumes that the distribution system has three attributes: i) it is
space-filling (i.e., it reaches all parts of the organism); ii) it minimizes the energy required for distribution;
and iii) it has size-invariant terminal units (e.g., capillaries or terminal xylem).
“From these assumptions we have derived a quantitative model for the geometry and physics of the entire
distribution system. The model predicts: i) a fractal-like branching network with scaling laws governing the
sizes of the branches; ii) whole-organism metabolic rate scales as M3/4; and iii) many other anatomical and
physiological characteristics of mammalian cardiovascular and respiratory systems (West et al. 1997).”
“The special fractal properties of biological resource distribution networks cause exchange surface areas to
scale as M3/4 and internal distances and transport times to scale as M1/4, rather than as M2/3 and M1/3 as
expected from conventional Euclidean geometry. This has many implications. For biology, it implies that
organisms exhibit ‘maximum fractality’ because they have been selected to be simultaneously maximally
powerful and maximally efficient.”
~ James H. Brown, “Scaling”, http://biology.unm.edu/jhbrown/Research/Scaling.html
bmr = cm3/4
bmr — basal metabolic rate; m — mass of organism; c — constant
This equation “is called Kleiber’s Law, and has been shown to be approximately true over 27 orders of
magnitude in the value of the mass, from the terminal oxidase molecules of the respiratory complex to
whales!
“Other relationships involving living organisms show similar scaling as the three-quarter power of the total
mass of the organism. Examples include brain mass.
“Other properties scale as the one-quarter or one-half power of the mass; examples include the heart rate
(-1/4), lifespan (1/4), unicellular genome lengths (1/4), and RNA concentration (-1/4).
“The fact that heart rate goes down as the body mass to the −1/4 power while lifespan goes up as the body
mass to the +1/4 power means that the number of heart beats in a lifetime is roughly constant independent
of the kind animal.”
~ Physics for the Life Sciences I
Circulatory System
“Unlike the genetic code, which has evolved only once in the history of life, fractal-like distribution
networks that confer an additional effective fourth dimension have originated many times. Examples include
extensive surface areas of leaves, gills, lungs, guts, kidneys, chloroplasts and mitochondria, the whole-
organism branching architecture of trees, sponges, hydrozoans, and crinoids, and the treelike networks of
diverse respiratory and circulatory systems … Although living things occupy a three-dimensional space,
their internal physiology and anatomy operate as if they were four-dimensional. Quarter-power scaling laws
are perhaps as universal and as uniquely biological as the biochemical pathways of metabolism, the
structure and function of the genetic code and the process of natural selection.”
~ West, G.B., Brown, J.H. and Enquist, B.J., “The Fourth Dimension of Life: Fractal Geometry and
Allometric Scaling of Organisms”, Science, Vol. 284, 1999, p. 1679
Isometric tension
“Most cells other than blood cells live within a fibrous extracellular matrix. Each cell is linked to this matrix
by proteins in its membrane called integrins, and the cell’s internal protein skeleton is constantly tugging on
these integrins to create a taut, tuned whole. “There’s isometric tension that you don’t see,” says Ingber
[head of Harvard University’s Wyss Institute for Biologically Inspired Engineering]. In practice, this means
changes in external tension — such as differences in the stiffness of the matrix, or the everyday stresses
and strains of normal muscle movement — can be transmitted into the cell and ultimately to the nucleus,
where they can direct the cell’s eventual fate.”
“For instance, if stem cells are exposed to flowing fluid, they turn into the endothelial cells that line the
inner surface of blood vessels. In fact, fluid flow — particularly pulses that mimic the effect of a beating
heart — is proving crucial for growing replacement arteries in the laboratory. The rhythmic stress helps
align the fibres of the developing artery, making them twice as strong, says Laura Niklason, a tissue
engineer at Yale University.”
“The growth of tissues like muscles, bone, skin and blood vessels has to be coordinated as our bodies
develop and adapt to different activities and injuries. A rigid genetic programme could easily be derailed,
whereas using tactile cues as guides allows tissues to adapt quickly as conditions change — for instance,
carrying heavy loads will make our bones grow stronger.
“This kind of plasticity may play a vital role in evolution as well as during the lifetime of individuals. When
the ancestors of giraffes acquired mutations that made their necks longer, for instance, they did not have to
evolve a whole new blueprint for making necks. Instead, the nerves, muscles and skin would have grown
proportionately without needing further changes in instructions. The result of this plasticity is a
developmental programme that is better able to cope with evolutionary changes, says Ingber.”
~ Bob Holmes, “Healing touch: the key to regenerating bodies”, New Scientist, 16 February 2010
E. The Natural History of Organisms
Arbitrariness of speciation:
Patchiness of biodiversity
“When scientists have attempted to remove a species from a territory, the population nevertheless remains
stable as animals from neighbouring territories fill in the gaps. Thus, it is not so much ‘nature red in tooth
and claw’ that keeps populations within bounds as it is that there’s an apparent natural size to a population,
just as there’s a natural size to an individual organism. The populations’ size depends on the way it is
related by feedback to the whole environment of other species and ecological resources.”
~ John Briggs and F. David Peat, Turbulent Mirror (Harper and Row, 1990), p. 158
“Norman Gilinsky of Virgina Polytechnic Institute … looked for evidence of the arrow [of time] in
‘clades,’ segments of the branches of the evolutionary tree whose thickness denotes diversity of species. He
found a decrease in the kinds of organic designs in the face of an increase in the number of species, an
asymmetry revealed by a ‘bottom heavy’ clade shape. He explains it as early experimentation, when
diversity quickly increases, and later standardization, when it tapers off and the organism wanes to
extinction. Gould believes it is the most outstanding trend of the fossil record.”
~ Peter Coveney & Roger Highfield, The Arrow of Time: A Voyage Through Science to Solve Time’s
Greatest Mystery (W.H. Allen, 1990), p. 254
“Extinction events remove a huge amount of biodiversity,” Coates [professor of organismal biology and
anatomy at the University of Chicago] said. “That shapes in a very significant way the patchiness of
biodiversity that persists to the present day.”
~ “Prehistoric Fish Extinction Paved the Way for Modern Vertebrates”, ScienceDaily, May 19, 2010
“…Gradualist-selectivist adaptationism characteristically depicts the evolutionary process as one of hill

climbing, not infrequently deploying … pleasant graphic artistry to convey the intuitions behind the model
of fitness landscapes and adaptive landscapes…. However, where there have been morphogenetic
explosions, fitness relations become surely non-transitive and plausibly irrelevant. There is no hill climbing,
not even a smooth path from each level of fitness to the next; only a jumpy traverse of a maze or a ‘glass-
like’ surface with a huge number of neighbouring peaks.”
No gradual divergence into niches

“Mark Pagel, an evolutionary biologist at the University of Reading, UK and his team gleaned more than
130 DNA-based evolutionary trees from the published literature [and] ended up with a list of 101 trees,
including various cats, bumblebees, hawks, roses and the like.
“Working with each tree separately, they measured the length between each successive speciation event,
essentially chopping the tree into its component twigs at every fork. Then they counted up the number of
twigs of each length, and looked to see what pattern this made. If speciation results from natural selection
via many small changes, you would expect the branch lengths to fit a bell-shaped curve.”
“Pagel’s team found that in 78 per cent of the trees, the best fit for the branch length distribution was
another familiar curve, known as the exponential distribution.”
Exponential curve indicates that speciation is triggered by a single accidental event.
“It isn’t the accumulation of events that causes a speciation, it’s single, rare events that falling out of
the sky, so to speak. Speciaition becomes an arbitrary, happy accident when one of these events
happens to you.”
~ Merk Pagel
“All kinds of rare events could trigger the accident of speciation. Not just physical isolation and major
genetic changes, but environmental, genetic and psychological incidents.”
The point is that this adaptation follows as a consequence of speciation, rather than contributing as a cause.
‘I think what our paper points to … is what could be, quite frequently, the utter arbitrariness of speciation.
It removes speciation from the gradual tug of natural selection drawing you into a new niche,’ he says.”
“Adaptive radiations” occur when “species seem to respond by diversifying into a host of new forms, each
adapted to a particular niche … pulled there by natural selection.” The highly variable rate of change would
yield a Bell curve with a lognormal distribution. But according to Pagel, this model “only works in about 6
percent of cases. It doesn’t seem to be a general way that groups of species fill out their niches.”
“This finding has independent support. Luke Harmon at the University of Idaho in Moscow and his
colleagues have examined 49 evolutionary trees to see whether there are bursts of evolutionary change early
in a group’s history, when unfilled niches might be expected to be most common. There is little evidence
for such a pattern, they report in the journal Evolution.”
“Over and over again, as biologists sequence the DNA of wild organisms, they find that what appears
superficially to be a single species is actually two, several or even many. The forests of Madagascar are
home to 16 different species of mouse lemurs, for example, all of which live in similar habitats, do similar
things, and even look pretty much alike. These cryptic species complexes are difficult to explain if
speciation is the end result of natural selection causing gradual divergence into different niches. But if new
species are happy accidents, there need be no ecological difference between them.”
~ Bob Holmes, “Accidental origins: Where species come from”, New Scientist, 10 March 2010
As Michael Kinnison of the University of Maine “puts it, the popular view of evolution is upside down.
People think evolutionary changes are imperceptible in the short term but add up to big changes over
millions of years. In fact, the opposite is true. It now appears that organisms evolve very rapidly in
response to any changes in their environment, but in the longer term most evolutionary changes cancel each
other out.”
“This is especially true of long periods with little or no evolutionary change. The conventional explanation
for this stasis has been that evolution is usually slow because selection is usually weak. ‘But this is
perfectly consistent with strong selection, providing it fluctuates,’says Graham Bell of McGill University in
Montreal, Canada.”
~ Michael Le Page, “Why evolution is going nowhere fast”, New Scientist, 05 April 2011
Weak or no effect by climate change
“Adaptationism certainly appears to hold true in microevolution — small-scale evolutionary change within
species, such as changes in beak shape in Galapagos finches in response to available food sources.
However, there is still huge debate about the role of natural selection and adaptation in ‘macroevolution’ —
big evolutionary events such as changes in biodiversity over time, evolutionary radiations and, of course,
the origin of species.”
“…The Earth has been on a long-term cooling trend for the past 65 million years. Superimposed upon this
are oscillations in climate every 20,000, 40,000 and 100,000 years caused by wobbles in the Earth’s orbit.
Over the past 2 million years — the Quaternary period — these oscillations have increased in amplitude and
global climate has lurched between periods of glaciation and warmer interglacials.”
“In the 1970s and 1980s, palaeoecologist Margaret Davis at the University of Minnesota in Minneapolis
created a map using this [pollen] data which showed how North American tree taxa reached their respective
present positions after the glaciers retreated at the end of the last ice age. She found that the distribution
shifts were individualistic, with huge variations between species in the rate, time and direction of spread.
For example, larch spread from south-west to north-east, white pine from south-east to north-west. Rates
vary from 100 metres a year to over 1000 metres (Annals of the Missouri Botanical Garden, vol. 70, p
550). In other words, trees show no predictable response to climate change, and respond individually rather
than as communities of species.”
“Research on animals has come to similarly unexpected conclusions, albeit based on sparser fossil records.
For example, palaeontologist Russell Graham at Illinois State Museum has looked at North American
mammals and palaeontologist Russell Coope at the University of Birmingham in the UK has examined
insects (Annual Review of Ecology and Systematics, vol. 10, p 247). Both studies show that most species
remain unchanged for hundreds of thousands of years, perhaps longer, and across several ice ages. Species
undergo major changes in distribution and abundance, but show no evolution of morphological
characteristics despite major environmental changes.”
“Molecular clock approaches allow us to estimate when two closely related modern species split from a
common ancestor by comparing their DNA. Most of this work has been carried out in birds, and shows
that new species appear more or less continuously, regardless of the dramatic climatic oscillations of the
Quaternary or the longer term cooling that preceded it (Trends in Ecology and Evolution, vol. 20, p 57).
“What of extinction? Of course, species have gone extinct during the past 20,000 years. However, almost
all examples involve some degree of human activity, either directly (think dodos) or indirectly (large
mammals at the end of the last ice age, 12,000 years ago).”
“The overall picture is that the main response to major environmental changes is individualistic movement
and changes in abundance, rather than extinction or speciation. In other words, the connection between
environmental change and evolutionary change is weak, which is not what might have been expected from
Darwin’s hypothesis.”
~ Keith Bennett, “The chaos theory of evolution”, New Scientist, 18 October 2010
Living space, not competition

…”PhD student Sarda Sahney and colleagues at the University of Bristol … used fossils to study
evolutionary patterns over 400 million years of history. Focusing on land animals — amphibians, reptiles,
mammals and birds — the scientists showed that the amount of biodiversity closely matched the availability
of “living space” [‘ecological niche concept’] through time.
“The new study [‘Links between global taxonomic diversity, ecological diversity and the expansion of
vertebrates on land,’ Biology Letters, 23 August 2010 vol. 6 no. 4 544-547] proposes that really big
evolutionary changes happen when animals move into empty areas of living space, not occupied by other
animals. For example, when birds evolved the ability to fly, that opened up a vast range of new possibilities
not available to other animals. Suddenly the skies were the limit, triggering a new evolutionary burst.
“Professor Mike Benton, a co-author on the study, explained that ‘competition did not play a big role in the
overall pattern of evolution. For example, even though mammals lived beside dinosaurs for 60 million
years, they were not able to out-compete the dominant reptiles. But when the dinosaurs went extinct,
mammals quickly filled the empty niches they left and today mammals dominate the land,’ he told BBC
News.”
~ “‘Survival of fittest’ is disputed”, BBC, 23 August 2010
“Drs. Jana Vamosi and Steven Vamosi of the Department of Biological Sciences at University of Calgary
“were looking at the underlying forces at work spurring diversity — such as why there could be 22,000
varieties of some families of flowers, orchids for example, while there could be only forty species of others,
like the buffaloberry family. In other words, what factors have produced today’s biodiversity?
“‘Our research found that the most important factor is available area. The number of species in a lineage is
most keenly determined by the size of the continent (or continents) that it occupies,’ says Jana Vamosi.
“Although geography may play a primary role, a close second is the flower morphology of the plants in a
particular family,” says Jana Vamosi. “So essentially all camps may claim partial victory because
morphological traits should be considered in the context of geographical area.”
~ “Toward Resolving Darwin’s ‘Abominable Mystery’: Patterns of Flower Biodiversity Point to the
Importance of Having ‘Room to Grow’”, ScienceDaily, Sep. 16, 2010
.....................................................................................................................
Survival of the Weakest:
“Conventional wisdom has it that for any given niche there should be a best species, the fittest, that will
eventually dominate to exclude all others. This is the principle of survival of the fittest. Ecologists often call
this idea the ‘competitive exclusion principle’ and it predicts that complex environments are needed to
support complex, diverse populations.”
Professor Robert Beardmore, from the University of Exeter, said: “Microbiologists have tested this
principle by constructing very simple environments in the lab to see what happens after hundreds of
generations of bacterial evolution, about 3,000 years in human terms. It had been believed that the genome
of only the fittest bacteria would be left, but that wasn’t their finding. The experiments generated lots of
unexpected genetic diversity.”
According to Professor Laurence Hurst, of the University of Bath, “Key to the new understanding is the
realization that the amount of energy organisms squeeze out of their food depends on how much food they
have. Give them abundant food and they use it inefficiently. When we combine this with the notion that
organisms with different food-utilizing strategies are also affected in different ways by genetic mutations,
then we discover a new principle, one in which both the fit and the unfit coexist indefinitely.”
Dr Ivana Gudelj, also from the University of Exeter, said “The fit use food well but they aren’t resilient to
mutations, whereas the less efficient, unfit consumers are maintained by their resilience to mutation. If
there’s a low mutation rate, survival of the fittest rules, but if not, lots of diversity can be maintained.”
~ “Evolution: Not Only the Fittest Survive”, ScienceDaily, Mar. 29, 2011
According to Timothy Taylor, an archaeologist and anthropologist at the University of Bradford, UK, “If
you wanted to kill something or to defend yourself, you don’t need a chipped stone tool — you can just
pick up a rock and throw it. With chipped stone, something else is going on, something called ‘entailment’:
using one thing to make another. You’re using some object to chip the stone into a particular shape with the
intention of using it for something else. There’s an operational chain — one tool entails another.
“Upright female hominins walking the savannah had a real problem: their babies couldn’t cling to them the
way a chimp baby could cling to its mother. Carrying an infant would have been the highest drain on
energy for a hominin female — higher than lactation. So what did they do? I believe they figured out how
to carry their newborns using a loop of animal tissue.”
“The archaeological record shows chipped stone tool technologies earlier than 2.5 million years ago. That’s
the smoking gun. The oldest fossil specimen of the genus Homo is at most 2.2 million years old. That’s a
gap of more than 300,000 years — more than the total length of time that Homo sapiens has been on the
planet. This suggests that earlier hominins called australopithecines were responsible for the stone tools.”
“Once you have slings to carry babies, you have broken a glass ceiling — it doesn’t matter whether the
infant is helpless for a day, a month or a year. You can have ever more helpless young and that, as far as I
can see, is how encephalisation took place in the genus Homo. We used technology to turn ourselves into
kangaroos. Our children are born more and more underdeveloped because they can continue to develop
outside the womb — they become an extra-uterine fetus in the sling. This means their heads can continue to
grow after birth, solving the smart biped paradox. In that sense technology comes before the ascent to
Homo. Our brain expansion only really took off half a million years after the first stone tools. And they
continued to develop within an increasingly technological environment.”
“Technology allows us to accumulate biological deficits: we lost our sharp fingernails because we had
cutting tools, we lost our heavy jaw musculature thanks to stone tools. These changes reduced our basic
aggression, increased manual dexterity and made males and females more similar. Biological deficits
continue today. For example, modern human eyesight is on average worse than that of humans 10,000
years ago.
“Unlike other animals, we don’t adapt to environments — we adapt environments to us. We just passed a
point where more people on the planet live in cities than not. We are extended through our technology. We
now know that Neanderthals were symbolic thinkers, probably made art, had exquisite tools and bigger
brains. Does that mean they were smarter?
“Evidence shows that over the last 30,000 years there has been an overall decrease in brain size and the
trend seems to be continuing. That’s because we can outsource our intelligence. I don’t need to remember
as much as a Neanderthal because I have a computer. I don’t need such a dangerous and expensive-to-
maintain biology any more. I would argue that humans are going to continue to get less biologically
intelligent.”
“The point is, the realm of artificial things — that is, technology — has a different generative pattern than
the Darwinian pattern of descent with modification…. Artificial objects are defined in terms of intention and
entailment — and that makes artificial things very different from biological things.”
“Humans are artificial apes — we are biology plus technology. We are the first creatures to exist in that
nexus, not purely Darwinian entities.”
~ Amanda Gefter, “Artificial ape man: How technology created humans”, New Scientist, 23 August 2010
“The brain in its modern form is about 200,000 years old, yet brain imaging shows reading taking place in
the same way and in the same place in all brains. To within a few millimetres, human brains share a reading
hotspot — what Stanislas Dehaene calls the ‘letterbox’ — on the bottom of the left hemisphere.
“Dehaene calls this the ‘neuronal recycling hypothesis’ … the idea that ‘human brain architecture obeys
strong genetic constraints, but some circuits have evolved to tolerate a fringe of variability’, Dehaene writes.
‘Part of our visual system, for instance, is not hard-wired, but remains open to changes in the environment.
Within an otherwise well-structured brain, visual plasticity gave the ancient scribes the opportunity to invent
reading.’”
“The area that reading co-opted originally evolved for the visual acuity needed to track animals, a skill with
obvious survival benefits. Some of the evidence for this comes from studying line, edge and curve detection
in the letterbox area, which also explains universal visual features of all alphabets.”
~ Owen Flanagan, “How our brains learned to read”, New Scientist, 23 November 2009
.....................................................................................................................
Nonintentionality:
“The salient difference between architects and the processes of evolutionary selection is that architects have
minds and evolutionary processes do not. Minds are useful things to have; it’s among their virtues that they
can represent things that didn’t happen; or things that happened a long time ago; or things that happened
far, far away; or things that will happen; or things that might happen; or that would happen if … , etc. This
includes, of course, counterfactual events and their counterfactual effects.” (p. 115)
“Many paradigm scientific theories are we think, best understood as historical narratives consider, inter alia,
theories about lunar geography, theories about why the dinosaurs became extinct, theories about the origin
of the Grand Canyon, or of the Solar System or come to think of it, of the Universe. All these projects (and
surely many others) are post-hoc searches for chains of sufficient causal conditions whose satisfaction
would explain the occurrence of the event in question. If we’re right adaptionist theories about how
heritable traits evolve are also of this kind.” (p. 137)
“To say that natural selection can’t distinguish between coextensive phenotypic traits is to say that it can’t
predict what would be the relative fitness of a phenotype that had one trait but lacked the other; it can’t tell
arches from spandrels.” (p. 154)
“To be sure, introducing mental states into the operation of natural selection would allow it to reconstruct
the distinction between selection and selection-for; and … that is just the distinction that a satisfactory
treatment of free-rider problems requires. But the cost would be catastrophic. Mental processes require
minds in which to happen. So to allow them in the theory of evolution would mean committing precisely
the error of which we’ve been accusing Darwin: construing natural selection on the model of selective
breeding. It ought to be common ground among naturalists that evolution is not an intentional process; it
isn’t run by Mother Nature or by Selfish Genes, or by the Tooth Fairy, or by God. Selective breeding is
something that somebody does. But natural selection is not; it is something that just happens.”
“Natural history isn’t a theory of evolution; it’s a bundle of evolutionary scenarios That’s why the
explanations it offers are so often post hoc and unsystematic.
“It’s in the nature of explanations in natural history to collapse across ontological levels. Maybe what
determines some aspect of a creature’s phenotype is the local weather or the composition of the local
atmosphere or the salinity of the local water or something about the creature’s biochemistry; or something
about the biochemistry of the creature’s prey; or maybe the creature’s relative size; or its relative weight; or
its buoyancy; or the colours of the things in its environment; or the density with which its environment is
populated, or the anatomy of its birth canal; or maybe it’s some aspect of the cosmic radiation that the
creature is subject to…. Or maybe it’s all of these acting at once. In short, practically anything about its
macrostructure or its microstructure or its internal environment or its external environment can play a role in
the fixation of a creature’s phenotype … Natural history is just one damned thing after another.” (p. 159)
“Marx and many other nineteenth-century luminaries notwithstanding, there is no level of historical
explanation; a fortiori, there is no theory of history. Rather, history is composed of many, many causal
chains, the links of which are wildly various, not just from the perspective of basic sciences like physics,
but also from the perspectives of the special sciences…. On the present view, Darwin made the same sort
of mistake that Marx did: he imagined that history is a theoretical domain; but what there is, in fact is only a
heterogeneity of causes and effects.” (p. 160)
“Here’s a metaphor that we prefer to Darwin’s: organisms ‘catch’ their phenotypes from their ecologies in
something like the way they catch their colds from their ecologies. The etiological process in virtue of
which phenotypes are responsive to ecologies is more like contagion than selection. There are at least two
respects in which this is so: one is that what diseases a creature catches depends not just on what kind of
world it inhabits but also, and probably ineliminably, on features of its endogenous structure: features
which it may have innately, or may have acquired in consequence of its prior interactions with its ecology.
Paramecia don’t catch colds, and our catching one cold doesn’t prevent us from catching another one.”
“Second, contagion depends, quite possibly ineliminably, on factors that work at very many different levels
of organization; and so, we thing, does the fixation of phenotypes. Part of the story about what happens
when one comes down with a cold concerns the microstructure of the pathogens and of one’s immune
system. Part of the story is about what having the virus does to the mucous membranes. And part of it is
about the age, sex, health, degree of exposure and so forth of the host. Clusters of facts of all of these sorts
(and no doubt of many others) contribute to the explanation of how and why we catch the colds we down
we do.” (p. 162)
~ Jerry Fodor and Massimo Piattelli-Palmarini, What Darwin Got Wrong (2010)

Evolution - Alpha and Omega

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— Alpha and omega

The Night Sky at the Dawn of the Solar System

1) ”A boundary is needed to separate life from non-life.”

Increasing genetic phase space

A casually anomalous process

“Let us call such situations causally anomalous…” (p. 134)

B. Development and Expression of the Genome

Regulatory sequences of HERVs include:

The Evolution of Biological Complexity:

The complexity of a single gene

A nested hierarchy of modules

C. Inheritance of Acquired Changes

The RCC1 chromatin protein interacting with the nucleosome.

Built-in randomness generator

D. From Genotype to Phenotype

Generating heritable phenotypes

“A phenotype is any observable characteristic or trait of an organism: such as its morphology,

Ernst Haeckel’s famous comparative analysis of vertebrate development

Complexity of form in rotolaria

“The ‘Belousov-Zhabotinsky reaction’ is a family of oscillating chemical reactions in which transition-metal

“…Gradualist-selectivist adaptationism characteristically depicts the evolutionary process as one of hill

No gradual divergence into niches

Living space, not competition

Survival of the Weakest:

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