Since Penman keeps asking me, and since he’s the only person who reads this blog apart from a few hundred spambots, here’s an attempt to summarise what James Shapiro is presenting in Evolution – a View from the 21st Century for a complete non scientist. Those with scientific training will realise it is grossly inadequate, but I’ve done a more critical review here!
As an overview, Shapiro is pro-naturalism and pro-evolution, but definitely anti-Neo-Darwinian in the sense that he gives evidence from the literature to suggest (a) that random mutation is an inadequate cause of variation and (b) that natural selection is an inadequate cause for that variation to be retained. His most radical, and therefore most controversial, claim is that both variation and selection are increasingly being shown to be processes directed by the cell for the organism’s benefit, rather than accidental changes that end up benefiting it fortuitously.
It would seem that he is restricting this view to what we see now in all cells – I assume he feels there was a time in the distant past when mutation and selection produced the beginnings of the sophisticated mechanisms we see now. Another way of putting this is that the ability to evolve in some sense “teleologically” is itself the product of evolution.
In PART 1 he starts with a “simple” example of the complex feedback controls cells use to determine how the genes are expressed under varying circumstances. He goes on to describe the multiple mechanisms there are to prevent copying errors and mutations, and how when mutation does occur it is in fact prompted by the cell. UV light, for example, doesn’t simply damage DNA. Instead, it first triggers extensive damage control mechanisms, and secondarily prompts particular patterns of mutations, which, he argues, are an attempt to produce adaptive mutations. By this and other example he shows that cell reproduction is very much more complex and orderly than is often thought.
Finally, in this section, he shows that Crick’s “central dogma”, which is that the flow of information must be strictly from the DNA code, through RNA, to the protein structures of the cell, is a gross oversimplication. Far from being a blue print consisting of “selfish genes” the genome is a database from which the cell selects information and which it can even edit.
This last theme is developed in PART II. He starts by expanding further on the complicated control circuits involved in DNA transcription and then gets on to epigenetics – those mechanisms that are not controlled by genes at all, but by other mechansisms in the cell. One example would be the way the cell “marks” genes either to be expressed (ie to work) or not, depending on needs including, in some cases, alterations in the environment. As such epigenetically-caused changes can last for at least several generations, it is a radical discovery because it sounds a bit like Lamarck’s idea of organisms changing in response to circumstances: the cell senses an altered environment, and edits the genome so that it changes what it does in the next generation.
Shapiro goes on to show the different functions being discovered in DNA (beyond the 1 gene = 1 protein stereotype). These include the complex processes involved in splicing different genetic sequences together, overlapping genes and so on, but also involve the controversial “junk DNA” – long repetitive sequences previously thought simply to be simply debris from viral attacks. Functions for these elements are either demonstrated or suggested, the upshot of which is that the cell has very many ways of switching and reordering genes, and that there appear to be mechanisms controlling what goes on, rather than random mutations. He feels justified in calling such a multi-level, complex and apparently controlled system of changes “natural genetic engineering.”
One illustrative example he cites is the mammalian immune system. This is designed to produce very large numbers of very specific kinds of mutations that can respond to many different attackers. It includes systems for refining the mutations that prove to be needed for ever-increasing effectiveness. The propostion is that if the immune system is able to direct “evolution” in such an orderly way, there is every reason to suppose it happens across the board in the process of evolution.
The section closes with the concept of “genome shock”, coined by his mentor Barbara McClintock, to describe the kinds of environmental stresses that can trigger “natural genetic engineering” and hence facilitate significant evolutionary changes. Environmental triggers that have been observed in bacteria and higher organisms include radiation, magnetic fields, temperature changes, overpopulation, starvation, trauma, day length and hybridisation (which can be a marker, of course, for loss of the usual mating opportunities from extinction).
PART III looks at some of the novel mechanisms for extensive genomic change found by gene sequencing, far beyond the point mutations of classical Neodarwinsim. Overall, says Shapiro, these indicate big, sudden (saltationary) changes over evolutionary history rather than the small, gradual changes of Darwinian theories. In other words, the fossil record reflects reality rather than being unrepresentative, as Darwin held. These mechanisms include horizontal gene transfer (major in bacteria, but maybe also significant via viral invasion in higher animals); the shuffling of whole chunks of the genome at once, rather than one base at a time (maybe producing novel proteins from bits of old ones); symbiogenesis (eg the sudden development of mitochondria and chloroplasts, but maybe also (according to the late Lynn Margulis) the incorporation of genetic material from parasites; possible hybridisation of disparate organisms (so that, eg, caterpillars and butterflies may reflect two different ancestral organisms); genome doubling at key evolutionbary stages; and the natural genetic engineering mechanisms described in the previous section, which may lead to changes as great as chromosome reorganisation events.
PART IV pulls everything together to suggest new ways of viewing and researching evolution. Shapiro’s first point is to promote systems biology – that is, looking at the organism as one would a complex inter-related computer system rather than in a reductionist way as a one-dimensional list of instructions. In effect, this involves changing from a concept of evolution as a series of accidents to that of evolution as a functional set of mechanisms. A RM & NS (or even a neutral theory of population genetics) is not going to be asking “How does the cell reorganise established functions to generate novelty?” or “How does the cell generate novel components” or “How does the cell re-use and modify old evolutionary inventions?” Another good question to ask would be whether “natural genetic engineering” does what it says on the tin – if an organism restructures its genome, does that actually provide evolutionary advantage? Do cells actually have the sophistication to do it (contra, Shapiro says, the Intelligent Design idea that they don’t – actually, ID might well welcome such mechanisms over chance, but would still be asking how the sophistication got there to begin with)?
Lastly, Shapiro suggests the possibility of being able to tie the mechanisms he has been describing at a molecular level into the grand history of earth’s evolutionary history. Can the apparent picture of evolutionary stasis, followed by bursts of change coinciding with global catastrophes like the KT event, be shown to fit with the way that cells actually respond to the kind of effects one would expect them to suffer in such events? That would be a question evolutionary theory hitherto has failed to address in a satisfactory manner.