The Origin of Species?
Despite the title of Darwin’s famous book, we cannot be sure to what extent natural selection acting on gradual accumulation of small mutations has accounted for the development of new species. Many of the examples that are often quoted as demonstrating that this is the main source of new species show that new species have arisen in new niches, e.g. by geographic isolation as in the case of the Galapagos island tortoises and finches. But this evidence, by itself, does not establish what the mechanism may have been. Other interpretations would also be possible.
Darwin’s idea of natural selection was in part based on observing the effects of artificial selection, producing many different varieties of dogs, cats, fish etc. But it is important to note that thousands of years of this kind of selection has produced new varieties, not fully-fledged new species as defined by inability to interbreed. At best, this demonstrates selection’s ability to produce incipient development of new species.
Perhaps the best example of species development is the variety of greenish warblers, forming what is called a ring species around the Himalayas. See http://www.zoology.ubc.ca/~irwin/greenishwarblers.html
Presumed evolution of Greenish Warblers around the Himalayas. The colours indicate the subspecies: Yellow: P. t. trochiloides; Orange: P. t. obscuratus; Red: P. t. plumbeitarsus; Green: P. t. “ludlowi”; Blue: P. t. viridanus.
From Wikimedia Commons. Wikipedia entry on Greenish Warblers
North of the Himalayas there are two varieties (subspecies?) that co-exist but do not interbreed. But they are each connected to varieties with which they do interbreed stretching around the Himalayas to join the ring together in the south. Ticehurst proposed in 1938 that the greenish warblers started in the south, then slowly evolved as they spread around the Himalayas to the west and east, to eventually meet in the north when they had become different species. Genetic data are consistent with his hypothesis. This is perhaps the best example we have of this process, which itself is rare. Note however that this evidence supports Ticehurst’s hypothesis about the historical development, since the two northern forms are the most distinct genetically, but it does not in itself prove the precise mechanism. It does not, for example, exclude a Waddington-type influence of the environment on the selection of combinations of genes, or any other process by which a Lamarckian process becomes assimilated into the genome. Nor does it exclude natural genetic engineering. This is a difficulty with any study of existing genetic variations to infer the process by which those variations originally arose. The role of natural genetic engineering could be determined when we have genome sequences from most or all of the varieties.
By contrast, hybridisation in plants readily generates new species, and the process of symbiogenesis must also have done so. Natural genetic engineering could also do so if it involves DNA shuffling that removes reproductive compatibility.
The important message here is not that the generation of new species by natural selection working on random mutations is impossible, but rather that the examples often quoted to prove that it happened are not so clear cut when they are examined closely. We have to distinguish evidence about the historical development of new species from evidence about the precise mechanisms by which this happened.
What are the implications for the speed of evolutionary change?
What are the implications for the speed of evolutionary change?
Some of the problems in evolutionary theory concern the speed of speciation. It is clear from the geological record that this has not always been smooth. One of the reasons why Cuvier disagreed with Lamarck in the early nineteenth century is that he was able to discredit Lamarck’s idea of the transformation of species by pointing to the fact that the fossil evidence, as it was known then, was also consistent with multiple periods of creation. The record was that patchy, and it was also clear that some species remained essentially unchanged for very long periods of time (stasis). In the twentieth century, with much more evidence to consider, Eldredge and Gould in 1971 proposed the theory of punctuated equilibrium to account for the fact that most fossil species show long periods of stasis, and that rapid (on a geological time scale) changes occurred more rarely and were important periods of speciation. The difference between their theory and that of Cuvier was that Eldredge and Gould were simply proposing that evolutionary change from a common ancestor does not happen at a constant speed, whereas Cuvier interpreted the evidence to show that there had been multiple creations.
Darwin also realised that evolutionary change could not always have been smooth. In the fourth edition of The Origin of Species he wrote “the periods during which species have undergone modification, though long as measured in years, have probably been short in comparison with the periods during which they retain the same form.” This is, in essence, Eldredge and Gould’s idea of punctuated equilibrium.
There has been much argument about what precisely is meant by ‘punctuated’. A gradual change over a hundred thousand or a million or even a few million years will appear rapid on a geological time scale of hundreds of millions of years. The Cambrian explosion that occurred over 500 million years ago is a good example. Within just 20 million years all the phyla in existence today had developed. The standard response to these kinds of theories has therefore been that they are entirely consistent with neo-darwinism. Changes in selection pressure due to environmental changes or geographic distribution, and the occasional catastrophic environmental change, might account for the observed variations in speed of change without supposing additional mechanisms of change.
The new evidence from work on symbiogenesis, the various forms of inheritance of acquired characteristics, genetic assimilation, natural genetic engineering, including genome change and reorganisation over and above the accumulation of chance mutations, changes the situation in more fundamental ways that require either extensions of or replacement of the modern synthesis. These mechanisms resemble punctuated equilibrium theories in proposing that evolution can occur in jumps. Since these can be very sudden indeed it is best to use a word different from ‘punctuated’ to avoid confusion with Eldredge and Gould’s theory. ‘Saltatory’ means jumping. The new mechanisms produce saltations of various kinds:
Symbiogenesis is the fusion of two species. The best established example of this is the bacterial origin of mitochondria and chloroplasts and, perhaps, other organelles. Clearly, this process is the ultimate in ‘saltation’. It depends on processes of cellular ingestion that are natural in the feeding activity of unicellular organisms and, on an evolutionary timescale, it is therefore very rapid indeed. Of course, subsequent changes can then also occur more slowly. We know, for example, that some of the ingested DNA in what became organelles eventually moved to the nucleus in eukaryotes.
See the film by Lynn Margulis on
http://www.voicesfromoxford.com/video/Homage-to-Darwin-part-2/63
Endosymbiosis: Homage to Lynn Margulis, a painting by Shoshanah Dubineer, occupies a hallway in the Morrill Science Center at the University of Massachusetts, Amherst, where Margulis was a professor until her death in 2011. Margulis maintained that genetic variation emerges primarily through symbiosis, not through competition.Click edit button to change this text.
Image courtesy of the artist, http://www.cybermuse.com
See also Evolution’s Other Narrative
Natural genetic engineering could also occur within a single generation. Reorganisations of genomes involving duplications, deletions and insertions of long sequences, would be essentially instantaneous on a geological timescale. Defenders of the modern synthesis have argued that speciation due to such changes, and symbiogenesis, should not be classified as punctuated equilibrium. That is correct in the sense that it was not what Eldridge and Gould had in mind. But so far as timescale is concerned such changes would be saltatory in the ordinary sense of the word. They would be even more sudden than the punctuations proposed by Eldredge and Gould.
Genetic assimilation can also occur rapidly. Waddington’s mid-twentieth century experiments showed that an induced acquired characteristic in fruit flies could become permanent (assimilated) within fourteen generations. This must have represented the time required for selection for an induced characteristic to bring together in a single genome all the relevant alleles for that characteristic to be passed on to subsequent generations without the inducing environmental stimulus. Waddington coined the term ‘epigenetics’ to describe his discovery. Today, epigenetics usually refers to genome and chromatin marking.
Inheritance of acquired characteristics through the persistence of epigenetic effects through successive generations can also speed up the evolutionary process. These transgenerational environmental influences should spread through a population much more rapidly since it is possible for a large fraction of the population to be subject to the same changes at the same time. There is no need to wait for a single DNA change to spread slowly through a population. The orthodox response to this mechanism is to dismiss it as transient, which it certainly is in some cases. But there are now examples of such transmission over many generations and which show the same degree of strength as standard genetic transmission. Since such effects would not need to occur very frequently, the difficulty in identifying them experimentally would be perfectly understandable. Speciation itself is a rare event.
While there can be considerable uncertainty about the relative contributions of the different mechanisms to evolutionary change, two conclusions seem clear. The first is that, with a variety of mechanisms open to the evolutionary process, the speed of evolution should be faster. The second is that it is probable that the relative contributions varied at different stages in evolution.
The language of neo-darwinism
This page answers the profound, and fundamental, question whether the language of neo-darwinism has been responsible for, and itself expresses, many of the problems with the way in which 20th century biology has been interpreted.
The short answer is ‘yes’. The discourse of neo-darwinism and twentieth century biology in general is intricately linked to the specific philosophical and scientific viewpoints that they represent. It is necessary to deconstruct this discourse since the associated concepts are not required by the scientific discoveries themselves. In fact it can be shown that no biological experiment could possibly distinguish even between completely opposite metaphorical interpretations. The discourse therefore forms an interpretive veneer that can even hide those discoveries in a web of interpretation.
It is also quite difficult to unravel since it is the whole discourse of neo-darwinism that is the problem. Each metaphor reinforces the overall mind-set until it is almost impossible to stand outside it and to appreciate how beguiling it is. Since it has dominated biological science for over half a century, the metaphysical viewpoint represented by this discourse is now so ingrained in the scientific literature that most biological scientists themselves probably don’t recognise its metaphysical nature. Most would probably subscribe to the view that it is merely an accurate description of what experimental work has shown: the discourse in a nutshell is that genes code for proteins that form organisms via a genetic program inherited by subsequent generations and which defines and determines the organism. What is wrong with that? The answer is that almost everything is wrong with it and, sadly, it is not required by the experimental science itself.
The approach used here is, first, to analyse the main metaphors individually, and then to show how they reinforce each other. At the end, I will ask ‘what could be an alternative and better discourse?’
The main problem words are ‘gene’, ‘selfish’, ‘code’, ‘program’, ‘blueprint’, ‘book of life’. We also need to examine secondary concepts like ‘replicator’ and ‘vehicle’.
‘Gene’
Neo-darwinism is a gene-centred theory of evolution. Yet its central entity, the gene, is an unstable concept. Surprising as it may seem, there is no single agreed definition of ‘gene’. Even more seriously, the different definitions have incompatible consequences for the theory.
The word ‘gene’ itself was coined by Johannsen in 1909, but the concept already existed and was based on “the silent assumption [that] was made almost universally that there is a 1:1 relation between genetic factor (gene) and character” (Mayr 1982). Since then, the concept of a gene has changed fundamentally, and this is a major source of confusion when it comes to the question of causation. Its original biological meaning referred to the cause of an inheritable phenotype characteristic, such as /hair/skin colour, body shape and weight, number of legs/arms/wings, to which we could perhaps add more complex traits such as intelligence, personality and sexuality.
The molecular biological definition of a gene is very different. Following the discovery that DNA forms templates for proteins, the definition shifted to locatable regions of DNA sequences with identifiable beginnings and endings. Complexity was added through the discovery of regulatory elements, but the basic cause of phenotype characteristics was still the DNA sequence since that determined which protein was made, which in turn interacted with the rest of the organism to produce the phenotype.
But unless we subscribe to the view that the inheritance of all phenotype characteristics is attributable entirely to DNA sequences (which is just false: DNA never acts outside the context of a complete cell) then genes, as originally conceived, are not the same as the stretches of DNA. According to the original view, genes were necessarily the cause of inheritable phenotypes since that is how they were defined. The issue of causation is now open precisely because the modern definition identifies them instead with DNA sequences.
The original concept of a gene has therefore been taken over and significantly changed by molecular biology. This has undoubtedly led to a great clarification of molecular mechanisms, surely one of the greatest triumphs of twentieth-century biology, and widely acknowledged as such. But the more philosophical consequences of this change for higher level biology are profound and they are much less widely understood.
The difference between the original and the molecular biological definitions of ‘gene’ can be appreciated by noting that most changes in DNA do not necessarily cause a change in phenotype. Organisms are very good at buffering themselves against genomic change. Further analysis of the difference between the definitions can be found in the answer on Slippery Definitions, which also includes an important diagram of the differences.
Some biological scientists have even given up using the word ‘gene’, except in inverted commas. As Beurton et al. (2008) comment “it seems that a cell’s enzymes are capable of actively manipulating DNA to do this or that. A genome consists largely of semi stable genetic elements that may be rearranged or even moved around in the genome thus modifying the information content of DNA.”
The reason that the original and the molecular biological definitions have incompatible consequences is that only the molecular biological definition could be compatible with a strict separation between the ‘replicator’ and the ‘vehicle’. A definition in terms of inheritable phenotypic characteristics (i.e. the original definition) necessarily includes more than the DNA, so that the distinction between replicator and vehicle is blurred.
‘Selfish’
As the lectures show, no possible biological experiment could conceivably distinguish between the selfish gene ‘theory’ and its opposites, such as prisoner or co-operative genes. See the answer What is wrong with The Selfish Gene. This point was conceded long ago by Richard Dawkins at the beginning of his book The Extended Phenotype: ‘I doubt that there is any experiment that could prove my claim’ (Dawkins, 1982, p. 1).
‘Code’
After the discovery of the double helical structure of DNA, it was found that each sequence of three bases in DNA or RNA corresponds to a single amino acid in a protein sequence (see What does DNA do?). These triplet patterns are formed from any combination of the four bases U, C, A and G in RNA and T, C, A and G in DNA. They are often described as the genetic ‘code’, but it is important to understand that this usage of the word ‘code’ is metaphorical and can be confusing.
A real code is an intentional encryption used by humans to communicate. The genetic ‘code’ is not intentional in that sense. The word ‘code’ has unfortunately reinforced the idea that genes are active causes, in much the same way as a computer program directs the computer to obey instructions. The more neutral word ‘template’ would be better. It also expresses the fact that templates are used only when required (activated); they are not themselves active causes. The active causes lie within the cells themselves since they determine the expression patterns for the different cell types and states. These patterns are communicated to the DNA by transcription factors, by methylation patterns and by binding to the tails of histones, all of which influence the pattern and speed of transcription of different parts of the genome. If the word ‘instruction’ is useful at all, it is rather that the cell instructs the genome. As the Nobel-prize winner, Barbara McClintock said, the genome is an ‘organ of the cell’, not the other way round.
Getting the direction of causality in biology wrong is a fundamental mistake with far-reaching consequences. These consequences include the frequent characterisation of genes as the genes ‘for’ this and that.
‘Program’
The idea of ‘le programme génétique’ (‘genetic program’) was first introduced by the French Nobel laureates, Jacques Monod and Francois Jacob. They specifically referred to the way in which early electronic computers were programmed by paper or magnetic tapes: “The programme is a model borrowed from electronic computers. It equates the genetic material with the magnetic tape of a computer” (Jacob 1982). The analogy was that DNA ‘programs’ the cell, tissues and organs of the body just as the code on a computer program determines what the computer does. In principle, the code is independent of the machine that implements it, in the sense that the code itself is sufficient to specify what will happen when the instructions are obeyed. If the program specifies a mathematical computation, for example, it would contain a complete specification of the computation to be performed in the form of complete algorithms. The problem is that no such algorithms can be found in the DNA sequences. What we find is better characterised as a mixture of templates and switches. The ‘templates’ are the triplet sequences that specify the amino acid sequences or the RNA sequences. The ‘switches’ are the locations on the DNA or histones where transcription factors, methylation processes and other controlling processes occur.
Since what we find in the genome sequences are templates and switches, where does the full algorithmic logic of a program lie? Where, for example, do we find the equivalent of ‘IF-THEN-ELSE’ type instructions? The answer is in the cell or organism as a whole, not just in the genome.
Take as an example circadian rhythm. The simplest version of this process depends on a gene that is used as a template for the production of a protein whose concentration then builds up in the cytoplasm. It diffuses through the nuclear membrane and, as the nuclear level increases, it inhibits the transcription process of its own gene. This is a negative feedback loop of the kind that can be represented as implementing a ‘program’ like IF LEVEL X EXCEEDS Y STOP PRODUCING X, BUT IF LEVEL X IS SMALLER THAN Y CONTINUE PRODUCING X. But it is important to note that the implementation of this ‘program’ to produce a 24 hour rhythm depends on rates of protein production by ribosomes, rate of change of concentrations within the cytoplasm, rate of transport across the nuclear membrane, and interaction with the gene transcription control site (the switch). All of this is necessary to produce a feedback circuit that depends on much more than the genome. It depends also on the intricate cellular, tissue and organ structures that are not specified by DNA sequences, which replicate themselves via self-templating, and which are also essential to inheritance across cell and organism generations.
This is true of all such ‘programs’. To call them ‘genetic programs’ is to fuel the misconception that all the logic lies in the one-dimensional DNA sequences. It doesn’t. It also lies in the three dimensional static and dynamic structures of the cells, tissues and organs.
The phrase ‘genetic program’ has therefore encouraged the idea that an organism is fully defined by its genome, whereas in fact it is also defined by its inheritance of cell structure as well as the genome. Moreover, this structure is specific to different species. Cross-species clones do not generally work, and when they do (very rarely) the outcome is determined both by the cytoplasmic structures as well as the DNA – see Immortal genes.
A debate on the motion “No privileged level of causation: An organism is not defined by its genome” was held in Leipzig in July 2012. Image below.
The protagonists were Sydney Brenner and Denis Noble. But the remarkable thing about this debate is that, on the central theme, they were both in agreement with the motion. There was no real debate!
‘Blueprint’
‘Blueprint’ is a variation on the idea of a program. Blueprints, for example as architectural designs for construction of buildings and other structures, existed before the modern idea of a computer program. The word suffers from a similar problem to the concept of a ‘program’, which is that it implies that all the information necessary for the construction of an organism lies in the DNA. This is clearly not true. The complete cell is also required, and its complex structures are inherited by self-templating. The ‘blueprint’, therefore, is the cell as a whole. But that destroys the whole idea of the genome being the full specification.
‘Book of Life’
The genome is often described as the ‘book of life’. This was one of the colourful metaphors used when projecting the idea of sequencing the complete human genome. It was a brilliant public relations move. Who could not be intrigued by reading the ‘book of life’ and unravelling its secrets? And who could resist the promise that, within about a decade, that book would reveal how to treat cancer, heart disease, nervous diseases, diabetes, with a new era of pharmaceutical targets. As we all know, it didn’t happen. Two editorials in 2010 (ten years after the first full draft of the human genome) spelt this out:
“Ten years ago, the first draft of the sequence of the human genome was heralded as the dawn of a new era of genetic medicine………. You might have noticed that it hasn’t [happened]. The medical impact of the human genome project (HGP) has so far been negligible.” (Editorial, Prospect, June 2010).
“The activity of genes is affected by many things not explicitly encoded in the genome, such as how the chromosomal material is packaged up and how it is labelled with chemical markers. Even for diseases like diabetes, which have a clear inherited component, the known genes involved seem to account for only a small proportion of the inheritance…… the failure to anticipate such complexity in the genome must be blamed partly on the cosy fallacies of genetic research. After Francis Crick and James Watson cracked the riddle of DNA’s molecular structure in 1953, geneticists could not resist assuming it was all over bar the shouting. They began to see DNA as the “book of life,” which could be read like an instruction manual. It now seems that the genome might be less like a list of parts and more like the weather system, full of complicated feedbacks and interdependencies.” (Editorial, Nature, 2010).
In response to these editorials I wrote (Noble 2012):
“In 2002 I wrote an article for the magazine of The Physiological Society, Physiology News, explaining why the genome is not the “Book of Life” (Noble, 2002). A reader was so enthused by it that he approached the Editor of Prospect to insist that it deserved a much wider readership and thought that Prospect was the ideal medium. It would have been, but the offer was turned down without question. Probably it didn’t fit the mind set of that time, full of confidence that molecular biology was going, finally, to deliver the goods through exploitation of the genome data.”
“What has changed in the subsequent 8 years, so that even a staff writer for Prospect now expresses the main message of the 2002 article? The answer is that 2010 is the ten year watermark after the sequencing of the genome, when we were promised by the leaders of the Human Genome Project that the benefits for health care would have arrived. Diabetes, hypertension and mental illness were amongst the targets. Science journalists are therefore becoming uneasy that they bought into a promise that has not and, I would argue, could not have been delivered. And they are not alone. The drug industry also bought in, literally so since start-up genomics companies were bought up for hundreds of millions of dollars. The sequencing of genomes has been of great value for basic science, particularly in studies on comparison of genomes for the purposes of evolutionary biology, but the interpretation of the genome data in terms of biological functions (phenotypes) has proved vastly more difficult than anticipated.”
‘The Book of Life’ represents the high watermark of the enthusiasm with which the discourse of neo-darwinism was developed. Its failure speaks volumes: the discourse was not only unnecessary, it was seriously misleading. Yes, there was a good scientific reason for sequencing whole genomes. The benefits to evolutionary biology in particular have been immense. But the discourse promising a peep into the ‘book of life’ and a cure for all diseases was a mistake.
The discourse as a whole
All parts of the discourse of neo-darwinism encourage the use and acceptance of the other parts. Once people have bought in to the idea that the DNA and RNA templates form a ‘code’, the idea of the ‘genetic program’ follows naturally. That leads on to statements like “they [genes] created us body and mind” (The Selfish Gene, 1976). In turn, that leads to the distinction between replicators and vehicles. The mistake lies in accepting the first step, the idea that there is a ‘code’.
The distinction between the replicator and the vehicle can be seen as the culmination of the neo-darwinist discourse. It follows on from accepting the ideas of a code and a program in the genome. If all the algorithms for the logic of life lie in the genome then the rest of the organism does seem to be a disposable vehicle. Only the genome needs to replicate, leaving any old vehicle to carry it.
The distinction however is a linguistic confusion and it is incorrect experimentally. It is a linguistic confusion since the word replicate means to reproduce. Cells also replicate in this sense. They also use templates to do so. The templates are the cell structures themselves. The process is therefore called self-templating and it is just as necessary and just as robust as genome replication. Indeed, faithful genome replication depends on the prior ability of the cell to replicate itself since it is the cell that contains the necessary structures and processes to enable errors in DNA replication to be corrected. See the answer Immortal genes?
The distinction is incorrect experimentally since cross-species cloning shows that cytoplasmic inheritance exists. Another way to make the same point is that the interpretation of the genome depends on the rest of the organism. To use the ‘program’ metaphor, the program is distributed between the genome and the cell.
Notice that the whole discourse is strongly anthropomorphic. This is strange, given that most subscribers to the discourse would wish to avoid anthropomorphising scientific discovery. As Dawkins wrote about the selfish gene metaphor: “I believe it is the literal truth.” When anthropomorphic language becomes confused with ‘literal truth’ we know we are in linguistic trouble.
An alternative discourse
Take some knitting needles and some wool. Knit a rectangle. If you don’t knit, just imagine the rectangle. Or use an old knitted scarf. Now pull on one corner of the rectangle while keeping the opposite corner fixed. What happens? The whole network of knitted knots moves. Now reverse the corners and pull on the other corner. Again the whole network moves. This is a property of networks. Everything ultimately connects to everything else. Any part of the network can be the prime mover, and be the cause of the rest of the network moving and adjusting to the tension.
Now knit a three-dimensional network. Again, imagine it. You probably don’t actually know how to knit such a thing. Pulling on any part of the 3 D structure will cause all other parts to move. It doesn’t matter whether you pull on the bottom, the top or the sides. All can be regarded as equivalent. There is no privileged location within the network.
The 3 D network recalls Waddington’s epigenetic landscape network (also shown here) and is quite a good analogy to biological networks since the third dimension can be viewed as representing the multi-scale nature of biological networks. Properties at the scales of cells, tissues and organs influence activities of elements, such as genes and proteins, at the lower scales. This is sometimes called downward causation, to distinguish it from the reductionist interpretation of causation as upward causation. ‘Down’ and ‘up’ here are also metaphors and should be treated carefully. The essential point is the more neutral statement: there is no privileged level (or scale) of causality. This is necessarily true in organisms which work through many forms of circular causality.
A more complete analysis of this alternative discourse can be found in the article on Biological Relativity, which can also be obtained by downloading the Sourcebook.
The important point about the alternative, relativistic, discourse proposed here is that all the anthropomorphic features of the neo-darwinist discourse can be eliminated, without changing a single biological experimental fact. There may be other discourses that can achieve the same result. It doesn’t really matter which you use. The aim is simply to distance ourselves from the metaphysical baggage that neo-darwinism has brought to biology, made all the worse by the fact that it has been presented as literal truth.
The great physicist, Poincaré, pointed out, in connection with the relativity principle in physics, that the worst philosophical errors are made by those who claim they are not philosophers. They do so because they don’t even recognise the existence of the metaphysical holes they fall into.
Is the proposed Integrative Synthesis really new?
The article proposes a new synthesis which differs in four major respects from the traditional (modern) synthesis:
But is this really a new proposal? Havn’t we heard about the demise of neo-Darwinism too often?
“The full extent of this feedback from function to inheritance remains to be assessed, but it cannot be doubted that it runs counter to the spirit of the Modern Synthesis. The challenge now is how to construct a new Synthesis to take account of this development. In Table 1, I call this the Integrative Synthesis. I believe that in the future, the Modern Synthesis and the elegant mathematics that it gave rise to, for example in the various forms and developments of the Price equation, will be seen as only one of the processes involved, a special case in certain circumstances, just as Newtonian mechanics remains as a special case in the theory of relativity.”
The problems with the modern synthesis are that it is restrictive and that it is dogmatic.
“What went wrong in the mid-20th century that led us astray for so long? The answer is that all the way from the Weismann barrier experiments in 1893 (which were very crude experiments indeed) through to the formulation of the central dogma of molecular biology in 1970, too much was claimed for the relevant experimental results, and it was claimed too dogmatically. Demonstrating, as Weismann did, that cutting the tails off many generations of mice does not result in tail-less mice shows, indeed, that this particular induced characteristic is not inherited, but it obviously could not exclude other mechanisms. The mechanisms found recently are far more subtle. Likewise, the demonstration that protein sequences do not form a template for DNA sequences should never have been interpreted to mean that information cannot pass from the organism to its genome. Barbara McClintock deservedly gets the last laugh; the genome is indeed an ‘organ of the cell’.”
The idea of a more nuanced multi-mechanism synthesis is indeed not new. I am delighted, for example, to acknowledge the similarity of my ideas to those of Eugene Koonin (2009), Messoudi et al. (2013) and Laland et al (2013). The problem is that the dogmatism of neo-Darwinism has prevented open admission of the change. The change has already happened in the minds of those who listen to the experimental evidence.
Eugene Koonin, The Origin at 150: Is a new evolutionary synthesis in sight? Trends in Genetics, 25, November 2009, pp. 473-475. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784144/
Eugene Koonin, Darwinian evolution in the light of genomics, Nucleic Acids Research, 37, 2009, pp. 1011-1034. http://www.ncbi.nlm.nih.gov/pubmed/19213802
Mesoudi A, Blanchet S, Charmentier A, Danchin E, Fogarty L, Jablonka E, Laland KN, Morgan TJH, Mueller GB, Odling-Smee FJ & Pojol B. (2013). Is non-genetic inheritance just a proximate mechanism? A corroboration of the extended evolutionary synthesis. Biological Theory 7, 189–195. http://link.springer.com/article/10.1007/s13752-013-0091-5
Laland, K. N., Odling-Smee, F. J., Hoppitt, W., and Uller, T. (2013) More on how and why: a response to commentaries, Biology and Philosophy DOI: 10.1007/s10539-013-9380-4.
Quotes from Koonin that resemble my text:
“In the post-genomic era, all the major tenets of the modern synthesis have been, if not outright overturned, replaced by a new and incomparably more complex vision of the key aspects of evolution.”
“The discovery of pervasive HGT [horizontal gene transfer] and the overall dynamics of the genetic universe destroys not only the tree of life as we knew it but also another central tenet of the modern synthesis inherited from Darwin, namely gradualism. In a world dominated by HGT, gene duplication, gene loss and such momentous events as endosymbiosis, the idea of evolution being driven primarily by infinitesimal heritable changes in the Darwinian tradition has become untenable.”
“The edifice of the modern synthesis has crumbled, apparently, beyond repair”.
“The exclusive focus of Modern Synthesis on natural selection acting on random genetic variation has been replaced with a plurality of complementary, fundamental evolutionary processes and patterns.”
Laland et al (2013) also express many of the same ideas, and it is particularly important to note that they have also pinpointed the concept of causation as one of the problems:
“We (like many other developmentally minded evolutionists, e.g. West-Eberhard 2003) believe that resistance to these ideas derives in part from implicit models of causation that can channel thinking on these topics, leading to the neglect of potentially important explanations. For instance, in their recent review of phenotypic plasticity’s impacts on speciation, where extensive evidence that plasticity is evolutionarily consequential was presented, Pfennig et al. (2010, p. 459) nonetheless conclude that “recent reviews of speciation generally fail to discuss phenotypic plasticity, indicating that workers in this field do not recognize a significant role for plasticity in speciation”.”
which may be compared to my article:
“A central feature of the Integrative Synthesis is a radical revision of the concept of causality in biology. A priori there is no privileged level of causation. This is the principle that I have called the theory of biological relativity (Noble, 2008, 2012)…… Control is therefore distributed, some of which is inherited independently of DNA sequences. The revision of the concept will also recognize the different forms of causality. DNA sequences are best viewed as passive causes, because they are used only when the relevant sequences are activated. DNA on its own does nothing. The active causes lie within the control networks of the cells, tissues and organs of the body.”
Laland et al also compare their position with the Modern Synthesis in the form of a table:
The compatibility of this table with my own is obvious. I do not claim any priority in expressing my ideas and I am delighted to discover others who see the evidence in much the same way. Where I have gone a little bit further is in pointing out how physiology comes back onto centre stage as the study of function: “the organism should never have been relegated to the role of mere carrier of its genes.”
Slippery definitions: how neo-darwinism accommodates contrary findings
There is a long history to this. There have been many points at which neo-darwinism has been challenged experimentally. The reactions can be characterised as a mixture of assimilation and denial.
An early example of assimilation is the reaction to the work of Conrad Waddington who first coined the term ‘epigenetics’. Waddington showed that an acquired characteristic in fruit flies could be assimilated after a number of generations of selection for the trait. After that it became inheritable in the standard way without the environmental stimulus that caused the character to be acquired. In the Experimental Physiology article I write
The Modern Synthesists should not have dismissed Waddington’s experiments, for example, as simply ‘a special case of the evolution of phenotypic plasticity’ (Arthur, 2010). Of course, the Modern Synthesis can account for the inheritance of the potential for plasticity, but what it cannot allow is the inheritance of a specific acquired form of that plasticity. Waddington’s experiments demonstrate precisely inheritance of specific forms of acquired characteristics, as he claimed himself in the title of his paper (Waddington, 1942). After all, the pattern of the genome is as much inherited as its individual components, and those patterns can be determined by the environment.
Notice that this also illustrates how neo-darwinism tends to be slippery when it defines a gene. Defining genes as individual protein-coding sequences ignores inheritance of characteristics that depend on the pattern of the genome. Waddington’s experiments show that it is perfectly plausible that a characteristic first arises through environmentally-induced change and then becomes ‘locked in’ to the genome pattern so that it becomes standard genomic inheritance. No mutations would be required and the characteristic could appear in a substantial fraction of the population rather than a single individual. We don’t know how often this process may have occurred during evolution. I suspect that many of the additional mechanisms of variation may become ‘locked in’ in this way.
A ‘gene’ in this sense can be a new combination of alleles that allows a new phenotype to develop. The mistake is to ‘atomise’ the concept of a gene. That is another important difference between the original definition in terms of phenotypes and the molecular biological definition in terms of ‘atomised’ DNA elements.
An example of what I would call denial is provided by an exchange during the 2009 Oxford debate that I chaired between Margulis and Dawkins. The transcript includes Dawkins’ reaction to the example of cellular inheritance independent of the genome in Paramecium:
“One example you might have meant is Sonneborn’s Paramecium where you cut a bit of the pellicle [ciliate cortex] and twist it ‘round. Well, if that’s true, and is indeed a non-DNA form of heredity, that’s absolutely fine. I would embrace that gladly as a new “honorary” gene. That’s fine. [Groans from the audience] Why not, why not?” (transcript, page 21)
The groans from the audience surely indicate something slippery here. I’d call it ‘having it both ways’. The whole point of the discussion was whether inheritance is determined by genes alone. Sure, we can go on redefining ‘gene’ until we have exhausted all the possibilities. But a statement that says everything also says nothing. The denial here is a denial of a counter-example to neo-darwinism by redefining what is meant by a gene. As I explain in the lectures the central confusion lies precisely in the slippage between defining genes as DNA sequences and their original definition in terms of inheritable phenotypes. Defined as the latter, there can, by definition, be no exceptions. Defined as the former, there clearly are exceptions.
The relevant slide in the lecture is:
Relations between genes, environment and phenotype characters according to current physiological and biochemical understanding This diagram represents the interaction between genes (DNA sequences), environment and phenotype as occurring through biological networks. The causation occurs in both directions between all three influences on the networks. This view is very different from the idea that genes ‘cause’ the phenotype (right hand arrow). This diagram also helps to explain the difference between the original concept of a gene as the cause of a particular phenotype and the modern definition as a DNA sequence. For further description and analysis of the ideas behind this diagram see Kohl et al. (2010) Clinical Pharmacology and Therapeutics 88, 25–33
The sense in which neo-darwinism has been falsified in this case is precisely that epigenetic inheritance shows that characteristics of the biological networks can be inherited independently of DNA. Examples of that are now rapidly accumulating.
Are these kinds of confusions still occurring? A recent example is provided by
Zuk et al (2012) The mystery of missing heritability: Genetic interactions create phantom heritability. PNAS, 109, 1193-1198.
which contains an equivalent to Dawkins’ invention of ‘honorary gene’ by inventing the term ‘phantom heritability’. In this case, the interactions that necessarily include the biological networks are apparently assimilated into standard genetics (hence the term ‘genetic interactions’), when in fact there must be much more inherited than the relevant DNA sequences. The authors write “In short, missing heritability need not directly correspond to missing variants, because current estimates of total heritability may be significantly inflated by genetic interactions.” The matter should not be closed off in this way since the question whether this does or does not involve inheritance of epigenetic effects must remain open to further experimentation. And it would be better to recognise this by avoiding terms like ‘genetic interactions’ that leave it unclear what precisely is involved but which also prejudice the conclusion in favour of standard genetic inheritance.
Redefinition of the central entity in neo-darwinism, i.e. the ‘gene’, leads to unintended consequences. Admitting ‘honorary’ or ‘phantom’ genes that refer entirely or partly to cytoplasmic inheritance makes nonsense of the distinction between ‘replicator’ and ‘vehicle’. The ‘vehicle’ becomes part of the ‘replicator’.
It is anyway! See Immortal genes.
New Synthesis or Extended Synthesis?
Even some of those who accept that we need to move on from the Modern Synthesis think that it would be simpler just to extend it by incorporating new experimental observations and the mechanisms they identify. So, would an Extended (Modern) Synthesis be sufficient? To the Modern Synthesis, we could add all the other mechanisms (inheritance of acquired characteristics, symbiogenesis, lateral gene transfer, etc) and call that the Extended Modern Synthesis.
I understand the motives, but there are several reasons why I did not opt for that way of presenting the change.
First, it is a central and specific feature of Neo-darwinism to exclude the inheritance of acquired characteristics. The Modern Synthesis took Darwin’s Natural Selection idea and added to it:
(1) the Neo-darwinist (NOT Darwinist) view that Lamarckism was impossible,
(2) that inheritance was entirely through Mendelian genes, and
(3) that variation in DNA is random in the sense that it is not directed by any functional processes.
In brief, the Neo-darwinian mechanism is that variations arise by chance, natural selection then works to see which of those variations win the competition to reproduce and dominate the gene pool of later generations. These assumptions are so fundamental to the Neo-darwinist view that it would be a strange hybrid to add to it precisely those mechanisms that it sought to exclude. It is more honest to say ‘we got it wrong’ by excluding them.
The analogy would be with the way in which Newtonian mechanics was replaced by relativity theory. It would have been absurd to call relativity theory Neo-newtonism! When experimental observations show precisely those processes that the theory did not predict, then we should say so. Somehow that needs to be recognised. Just as the Neo-darwinists saw themselves as developing a new theory by integrating Mendelian genetics with natural selection, we now need in some way to recognise that nature is even more wondrous than they thought, and involves processes we thought were impossible.
Second, it is important for historical reasons to recognise the injustices done to Lamarck, Waddington, McClintock, Margulis …….and many others. The dogmatic way in which Neo-darwinism was promulgated damaged reputations, it damaged careers, and it damaged whole disciplines which, like physiology, were excluded from contributing to the concepts of evolutionary biology. In my view, it even affected the reputation of Charles Darwin. Darwin was far from being a Neo-darwinist. He included the inheritance of acquired characteristics in his Origin of Species, even formulated his own mechanism (his theory of gemmules), and he acknowledged Lamarck in glowing terms: “this justly celebrated naturalist….who upholds the doctrine that all species, including man, are descended from other species.” (Preface to the 4th edition of The Origin of Species, 1866).
Third, there is the problem of nomenclature. Neo-darwinists, by using that term, captured the glow of Darwin’s name, but they do not always clearly distinguish whether they are talking about Darwinism or Neo-darwinism. This is the reason why criticisms of Neo-darwinism are often interpreted as criticism of Darwin. As Waddington knew well, it is perfectly possible to be a Darwinist without being a Neo-Darwinist. In the article I write:
“I start with some definitions. I will use the term ‘Modern Synthesis’ rather than ‘Neo-Darwinism’. Darwin was far from being a Neo-Darwinist (Dover, 2000; Midgley, 2010), so I think it would be better to drop his name for that idea. As Mayr (1964) points out, there are as many as 12 references to the inheritance of acquired characteristics in The Origin of Species (Darwin, 1859) and in the first edition he explicitly states ‘I am convinced that natural selection has been the main, but not the exclusive means of modification’, a statement he reiterated with increased force in the 1872, 6th edition.”
These considerations lead to the following conclusions:
- It would be better to drop the name ‘Neo-darwinism’ in describing what replaces it.
- The Modern Synthesis incorporates Neo-darwinism, which is why I incline towards dropping this name also. But, if we are to refer to an extended synthesis, Extended Modern Synthesis would be better than Extended Neo-darwinism since combining Neo-darwinism with Lamarckism would be a stark contradiction.
- I prefer the term ‘Integrative Synthesis’ since it highlights the fact that it would be an integration of many mechanisms, each playing roles whose importance can vary at different stages of the evolutionary process, and each of which can interact with the others. This would be a genuinely systems biological view of evolution, emphasising those interactions.
What replaces the Modern Synthesis will necessarily be a hybrid incorporating different mechanisms. I suspect that the only common feature will be that evolution happened.
These points can also be explained using a development of a valuable diagram from Pigliucci and Müller. Click on the movie below
The movie shows the transformation from Piggliucci and Müller’s figure to the one below:
Diagram developed from Pigliucci, M., and Müller, G. B. (2010) Evolution – The extended synthesis, MIT Press, Cambridge, Mass.
The central circle represents the main features of Darwinism. The left hand ellipse represents most of the additional features of neo-darwinism (modern synthesis). The right hand ellipse represents the proposed extension.
My view is that the extension can best be represented as an extension of Darwinism. Nearly everything added is compatible with the original Darwinist assumptions. The main exception is that genomic evolution includes lateral transfer which modifies the Darwinian ‘tree of life’ to become a ‘network of life’.
The difficulties with representing the extension as one of neo-darwinism is that there are several negative characteristics of neo-darwinism that are not specifically referred to but which make it difficult from a historical point of view to see neo-darwinisn as the base for the extension. As explained above, neo-darwinism explicitly excluded the inheritance of acquired characteristics, denied the role of processes of genome change other than by chance, excluded symbiogenesis, and embraced the central dogma. All these need to be abandoned. The coloured items in my version of the diagram indicate some of the features that are in direct contradiction to neo-darwinism.
Since writing this page in 2013 I have been able to check with one of the authors of the Extended Evolutionary Synthesis who confirms that they also see it as a replacement not as a simple extension of neo-Darwinism.
Does the 2013 article criticise Darwinism?
No. Not really. In fact the main thrust of the article is a return to a less dogmatic view which is more in keeping with Darwin’s original ideas.
“In some respects, my article returns to a more nuanced, less dogmatic view of evolutionary theory (see also Müller, 2007; Mesoudi et al. 2013), which is much more in keeping with the spirit of Darwin’s own ideas than is the Neo-Darwinist view.”
Müller GB (2007). Evo–devo: extending the evolutionary synthesis. Nat Rev Genet 8, 943–949. http://www.ncbi.nlm.nih.gov/pubmed/17984972
Mesoudi A, Blanchet S, Charmentier A, Danchin E, Fogarty L, Jablonka E, Laland KN, Morgan TJH, Mueller GB, Odling-Smee FJ & Pojol B. (2013). Is non-genetic inheritance just a proximate mechanism? A corroboration of the extended evolutionary synthesis. Biological Theory 7, 189–195. http://link.springer.com/article/10.1007/s13752-013-0091-5
“One of the major developments of Darwin’s concept of a ‘tree of life’ is that the analogy should be more that of a ‘network of life’ (Doolittle, 1999; Woese & Goldenfeld, 2009).”
DoolittleWF (1999). Phylogenetic classification and the universal tree. Science 284, 2124–2128. http://www.ncbi.nlm.nih.gov/pubmed/10381871
Woese CR & Goldenfeld N (2009). How the micobial world saved evolution from the Scylla of molecular biology and the Charybdis of the modern synthesis. Microbiol Mol Biol Rev 73, 14–21. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650883/
The network represents the evidence for extensive exchange of DNA that must have occurred in the early stages of evolution, but which also continued through later stages.
The main departure from Darwin’s ideas is that the ‘tree of life’ is a network:
What explains the dogmatism and persistence of neo-darwinism?
When the history of neo-Darwinism gets written it will need to answer this question. I am not a historian. The answers I give here are tentative. They could be leads for serious historians of science to follow up. I also highlight two brilliant scientists, Waddington and McClintock, whose work should not have been neglected.
The progress of science is not Popperian
Despite the great influence of Popper, single contrary observations rarely destroy a strongly established theory. The tendency is to fix theories, extend them, even to redefine their entities, in ways that allow the contrary observations to be absorbed. This is what happened to Waddington’s work. If they can’t be absorbed in this way, they are sidelined as anomalies. This nearly happened to McClintock until she was awarded the Nobel Prize for discovering mobile genetic elements (jumping genes). It is more often the accumulation of many forms and examples of contrary evidence that persuades people to change. I think we are at that point now in the case of neo-Darwinism. There are exceptions to all the central assumptions, and in the case of the inheritance of acquired characteristics the exceptions are becoming a flood of evidence. Moreover, the central element of the theory, the gene, is no longer easy to define. All those functional RNAs also act as ‘genes’. The marking of the genome and chromatin also play a role in inheritance. That is the reason why a growing number of scientists admit that a major rethink is already happening.
Conrad Waddington in 1946 (left, from The Royal Society picture library) and his diagram of the epigenetic landscape (right, from The Strategy of the Genes, 1957). Genes (solid pegs at the bottom) are viewed as parts of complex networks so that many gene products interact to produce the phenotypic landscape (top) through which development occurs. Waddington’s insight was that new forms could arise through new combinations to produce new landscapes in response to environmental pressure, and that these could then be assimilated into the genome. Waddington was a systems biologist in the full sense of the word. If we had followed his lead many of the more naïve 20th century popularizations of genetics and evolutionary biology could have been avoided.
Left: Barbara McClintock in her laboratory in 1947 (Smithsonian Institute Archives).
“In the future attention undoubtedly will be centered on the genome, and with greater appreciation of its significance as a highly sensitive organ of the cell, monitoring genomic activities and correcting common errors, sensing the unusual and unexpected events, and responding to them, often by restructuring the genome. We know about the components of genomes that could be made available for such restructuring. We know nothing, however, about how the cell senses danger and instigates responses to it that often are truly remarkable.” (McClintock, Barbara. 1984 The significance of responses of the genome to challenge. Science 226, 792-801.)
McClintock clearly understood the correct direction of causality in relation to the genome. Characterising the genome as “a highly sensitive organ of the cell” was her great insight. It is as foolish to regard the genome as the active cause of the organism as it would be to say that the pipes of an organ play the music!
Right: giving Nobel Prize lecture in 1983 (NIH)
Cold War
Theories of evolution became an issue during the Cold War. Those, like Waddington, who found evidence for the inheritance of acquired characteristics were thought in some way to be associated with Lysenkoism, a Soviet era school that denied Mendelian inheritance. Waddington was not even allowed to visit the USA. His work was virtually ignored in the USA, and was eventually sidelined in the UK. He saw himself as a Darwinist, but not as a neo-Darwinist. I think it is shameful that such a brilliant scientist was side-lined, just as I think it is shameful that Lamarck was virulently denigrated. Anyone who thinks that science is neutral, and is not influenced by politics, should answer the question: how did these injustices happen?
See also http://musicoflife.website/pdfs/LetterfromLamarck.pdf
Religious fundamentalism
It is said that nearly 50% of the population of the USA do not accept the theory of evolution. Some are called creationists since they believe in various forms of creation, either literally as described in Genesis, or in a variety of more modern ideas of creationism. Some also espouse the ideas of Intelligent Design (ID). Both the creationists and the supporters of ID tend to take every example of a break with neo-Darwinism as a vindication of their views. Some have done the same with my article, despite the fact that I make it clear that I am arguing for a return to a “more nuanced, less dogmatic view of evolutionary theory (see also Muller, 2007; Mesoudi ¨ et al.2013), which is much more in keeping with the spirit of Darwin’s own ideas than is the Neo-Darwinist view.”
Muller GB (2007). Evo–devo: extending the evolutionary synthesis. Nat Rev Genet 8, 943–949 http://www.ncbi.nlm.nih.gov/pubmed/17984972
Mesoudi A, Blanchet S, Charmentier A, Danchin E, Fogarty L, Jablonka E, Laland KN, Morgan TJH, Mueller GB, Odling-Smee FJ & Pojol B. (2013). Is non-genetic inheritance just a proximate mechanism? A corroboration of the extended evolutionary synthesis. Biological Theory 7, 189–195. http://link.springer.com/article/10.1007/s13752-013-0091-5
One way to view the dogmatic nature of neo-darwinism as it is often presented in public is to see it as a reaction to the dogmatism of the creationists. The ‘uncertain’ (in the sense of lacking reason) faith in creationism is replaced by the ‘certainties’ of science. But there is a conflation here of very different degrees of certainty in science. There can’t be much doubt about the fact that life on earth has evolved. There is much less certainty about the mechanisms. Unlike Darwinism (Darwin knew nothing of mechanisms, genes were not known), neo-darwinism proposes the exclusion of many mechanisms that have in fact now been found to occur in nature. Adopting the ‘certainty’ of evolution to clothe the ‘uncertainty’ of particular theories about mechanisms has been the cause of many problems in public debate on evolution. It is perfectly possible to defend the virtual certainty that life has evolved while debating in the usual argumentative scientific way the uncertainties surrounding the question of mechanisms. The truth is that amongst the many mechanisms now known we know very little about which were prevalent in evolution. The answer is likely to be that different mechanisms were dominant at different stages. Evolution itself evolves.
See also the item on The Language of Neo-darwinism where the discourse of neo-darwinism is analysed.
What does DNA do?
Table of the nucleic acid template patterns for the formation of amino acids in protein sequences (from wikipedia). These triplet patterns are formed from the four bases U (uracil in RNAs), T (thymine in DNA), C (cytosine), A (adenine), and G (guanine), and are often described as the genetic ‘code’, but it is important to understand that this usage of the word ‘code’ is metaphorical and can be confusing. A real code is an intentional encryption used by humans to communicate. The genetic ‘code’ is not intentional in that sense. The more neutral word ‘template’ is better. It also expresses the fact that templates are used only when required (activated), they are not themselves active causes.
DNA sequences are templates for the formation of RNAs, some of which are in turn used as templates for the formation of proteins. Only RNAs and proteins are specified by the DNA sequences. RNAs and proteins then cooperate with many metabolites and other components of the organism to generate the numerous interlocking biochemical pathways. These pathways in turn work within the three dimensional structure of the cells, tissues and organs of the body. But this three-dimensional structure is not to be found in the one-dimensional DNA sequences. How then do cells know how to form such an intricate biological mechanism of precise functionality? The answer is self-templating. The three-dimensional structures copy themselves, first by growing in size and then, when the cell becomes large enough to divide, the structures are divided between the two cells. Each daughter cell therefore inherits its complete complement of structure as well as inheriting the genome.
For further aspects of the answer to this question see Immortal genes?
What is a template?
In the item The Language of Neo-darwinism I refer to DNA sequences as templates rather than as code. What is a template and why do I think that is a better metaphor?
I am the fortunate owner of three classical guitars made by the top English luthiers, David Rubio and Paul Fischer. David Rubio made guitars for Julian Bream and the label of one of my Rubios is signed by Bream. I inherited this guitar by buying it from my guitar teacher.
Guitar made by Paul Fischer with uniform fine-grained cedar for the soundboard
Needless to say, these guitars are a joy to play. I am not really a good enough performer for them but I love being able to play them. Like inheriting a good genome from your parents, it helps with life, it gives you a head start!
Why are these guitars so good? All top luthiers select the wood very carefully and season it correctly. The soundboard must have an almost perfectly uniform grain. But this is not all. The soundboard resonance properties are also determined by struts that are placed on the underside of the wood, inside the guitar and hidden from view. The pattern of these struts is unique to each luthier. In their striving to combine sweet tone with increased volume, they experiment extensively with exactly how the struts should be placed.
Recently, I acquired the template that Paul Fischer used to ensure that his struts follow his designed pattern. He has now retired from guitar making and no longer needs it. The template is for a fan strut pattern, which is characteristic of his guitars
The precise placing of these fan struts (braces) determines the balance between the resonances of the wood at different frequencies. In a sense therefore the template used is a cause of the way in which the instrument plays. So also is the way in which the guitarist strikes the strings. Even the shape, length and smoothness of the fingernails are important. But clearly we are dealing here with different kinds of cause. The template is a passive cause. Its existence and use were necessary but in no sense can the template be said to play the music. The active cause of the music that the instrument produces is the act of playing by the guitarist. This distinction between active and passive causes is important.
This is the distinction that is ignored when people say that their genes ‘made them … body and mind’. The genome is our template. Our protein networks within the cells and organs of the body are our guitar. But we play the music of life.
The genome sequences work just like Fischer’s template. They determine how my body’s proteins are structured. But they do not themselves carry out the physiological functions served by proteins, metabolites and the three-dimensional cellular and organ structures within which they work.
It’s as simple as that.
With thanks to Paul Fischer
Luthier extraordinaire
Does evolution evolve?
It must have done so.
The neo-darwinist process is a late comer since it is unlikely to have been the main mechanism before the development of multicellular organisms with separate specialised germline cells. It is a zoology-orientated view of evolution. Zoological organisms have existed for only about 20% of the duration of life on earth.
Similarly, inheritance via DNA cannot have occurred before the evolution of DNA. Sexual selection and mixing mechanisms cannot have evolved before the mechanisms for fusing, dividing and recombining genomes.
The evolution of the cell probably occurred before that of DNA, and certainly before DNA organised into genomes.
In fact, the list of stages is almost endless. The organisation of genomes, particularly genomes with chromatin and enclosed in a nucleus, must have occurred in many stages.
Not only does evolution evolve, so does the context in which it happens since it also changes the environment. New niches are created by evolution which can then be the context for new forms to evolve. It is an endless wondrously intricate web of contexts, structures and mechanisms. It can’t be reduced to a simple formula with one paradigmatic mechanism.
Laland, KN, Odling-Smee, J, Feldman, MW, Kendal, J. (2009) Conceptual Barriers to Progress Within Evolutionary Biology. Found Sci 14, 195-216 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093243c
Odling-Smee, F. J., Erwin, D., Palkovacs, E. P., Feldman, M. W., and Laland, K. N. (2013) Niche Construction Theory: a practical guide for ecologists, The Quarterly Review of Biology 88, 4-28. http://www.ncbi.nlm.nih.gov/pubmed/23653966
“It’s highly plausible, it’s economical, it’s parsimonious, why on earth would you want to drag in symbiogenesis when it’s such an unparsimonious, uneconomical [theory]?”
Margulis replied:
“Because it’s there.”
That’s it in a nutshell. What is there, what exists, which is the starting point of all science.
See
http://www.voicesfromoxford.org/video/Homage-to-Darwin-part-1/74
http://www.voicesfromoxford.org/video/Homage-to-Darwin-part-2/63
http://www.voicesfromoxford.org/video/Homage-to-Darwin-part-3/75
for the debate
http://musicoflife.website/pdfs/HOMAGE_COMMENTARY_Music%20of%20Life.pdf for a commentary
An image from the series of three videos recording the 2009 debate on the Voices from Oxford website. Click on the image to access the videos.
See also Two Wrongs for more information on Lynn Margulis and the way in which her major contributions to the theory of evolution have been denigrated. Yet the transition to cells with mitochondria or chloroplasts was surely an absolutely fundamental step in evolution.
Jean-Baptiste Pierre Antoine de Monet, Chevalier de la Marck
Jean-Baptiste Pierre Antoine de Monet, Chevalier de la Marck This is the person usually called Lamarck. He was born in 1744, before the French Revolution. He became Professor at the famous Jardin des Plantes in Paris, where the museums contained a rich collection of geological objects gathered from all over the world. He was initially strongly opposed to the idea of evolution, but his studies of these objects convinced him that the earth was far older than people thought, and that the geological evidence showed that species had changed. It was in 1800 that he delivered a lecture in which he championed his theory of transformationism (transmutation), and in 1809 he published his greatest work, Philosophie Zoologique, in which this theory was elaborated.
Lamarck’s achievements are remarkable:
- He was one of the first to use the term ‘Biology’ to describe the subject. He argued that living organisms had properties that were unique but that these were the outcome (today we would say emergent properties) of the physics and chemistry of matter. He was a materialist, but one who realised that the characteristic of living organisms was their organisation and structure, not just their components.
- He thought that all organisms had developed from tiny sea creatures. He therefore had a version of the common ancestor idea.
- He saw that there was a direction in the evolutionary process towards greater complexity. This led him to the concept of ‘le pouvoir de la vie’ (the force of life).
There were precursors of Lamarck, just as Lamarck himself was a precursor of Darwin. But Lamarck should be recognised as one of the key scientists in the development of evolutionary biology. Darwin fully recognised this status: “this justly celebrated naturalist….who upholds the doctrine that all species, including man, are descended from other species.” (Preface to the 4th edition of The Origin of Species, 1866).
Several developments led to the blackening of his name.
- He championed, but did not invent, the idea that acquired characteristics could be inherited. That itself would have been fine. Darwin also accepted this idea. The problem was that the subsequent establishment of the Weismann barrier (isolation of the germ line) and then the Central Dogma (isolation of the genome) led to the idea being so completely ridiculed that Lamarck’s reputation was ruined.
- ‘Le pouvoir de la vie’ was often interpreted to mean belief in a special ‘vital force’. My reading of his work is that he certainly did not intend this interpretation. He was a materialist, not a vitalist.
- His great rival, Georges Cuvier, opposed the idea of evolution and wrote a devastating criticism of Lamarck, which was used at his funeral.
http://www.victorianweb.org/science/science_texts/cuvier/cuvier_on_lamarck.htm
The historian of Science, Pietro Corsi, has created a superb on-line resource on Lamarck:
I wrote an imagined letter from Lamarck:
http://musicoflife.website/pdfs/LetterfromLamarck.pdf
which expresses the reasons why I think he has been badly treated.
These books by Eva Jablonka and her co-authors/editors are also valuable resources, particularly on the various mechanisms by which ‘lamarckian’ inheritance occurs:
Jablonka, E. and M. Lamb (1995). Epigenetic inheritance and evolution. The Lamarckian dimension. Oxford, OUP.
Jablonka, E. and M. Lamb (2005). Evolution in Four Dimensions. Boston, MIT Press.
Gissis, S. B. and E. Jablonka, Eds. (2011). Transformations of Lamarckism. From Subtle Fluids to Molecular Biology. Cambridge, Mass, MIT Press.
Links to video lectures and the Sourcebook
(100 pages – all the evidence and references – free of charge)