Michael Skinner writes: The unifying theme for much of modern biology is based on Charles Darwin’s theory of evolution, the process of natural selection by which nature selects the fittest, best-adapted organisms to reproduce, multiply and survive. The process is also called adaptation, and traits most likely to help an individual survive are considered adaptive. As organisms change and new variants thrive, species emerge and evolve. In the 1850s, when Darwin described this engine of natural selection, the underlying molecular mechanisms were unknown. But over the past century, advances in genetics and molecular biology have outlined a modern, neo-Darwinian theory of how evolution works: DNA sequences randomly mutate, and organisms with the specific sequences best adapted to the environment multiply and prevail. Those are the species that dominate a niche, until the environment changes and the engine of evolution fires up again.
But this explanation for evolution turns out to be incomplete, suggesting that other molecular mechanisms also play a role in how species evolve. One problem with Darwin’s theory is that, while species do evolve more adaptive traits (called phenotypes by biologists), the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed. Scientists, well-aware of the issue, have proposed a variety of genetic mechanisms to compensate: genetic drift, in which small groups of individuals undergo dramatic genetic change; or epistasis, in which one set of genes suppress another, to name just two.
Yet even with such mechanisms in play, genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change for a host of traits, from adjustments in metabolism to resistance to disease. The rapid emergence of trait variety is difficult to explain just through classic genetics and neo-Darwinian theory. To quote the prominent evolutionary biologist Jonathan B L Bard, who was paraphrasing T S Eliot: ‘Between the phenotype and genotype falls the shadow.’
And the problems with Darwin’s theory extend out of evolutionary science into other areas of biology and biomedicine. For instance, if genetic inheritance determines our traits, then why do identical twins with the same genes generally have different types of diseases? And why do just a low percentage (often less than 1 per cent) of those with many specific diseases share a common genetic mutation? If the rate of mutation is random and steady, then why have many diseases increased more than 10-fold in frequency in only a couple decades? How is it that hundreds of environmental contaminants can alter disease onset, but not DNA sequences? In evolution and biomedicine, the rates of phenotypic trait divergence is far more rapid than the rate of genetic variation and mutation – but why?
Part of the explanation can be found in some concepts that Jean-Baptiste Lamarck proposed 50 years before Darwin published his work. Lamarck’s theory, long relegated to the dustbin of science, held, among other things, ‘that the environment can directly alter traits, which are then inherited by generations to come’. [Continue reading…]
