One Less Gap for the 'God of the Gaps'
The “God of the gaps” just got squeezed out of yet another dwelling place.
This centuries-old argument for the existence of God basically goes like this. There is no way to explain (fill in the blank: lightning . . . volcanoes . . . the creation of the sun and planets . . . the origin of species . . . ) without invoking a supernatural hand; science alone falls short. Hence there must be a God. The trouble, of course, is that science has this annoying habit of eventually accounting for such mysteries through natural, not supernatural, processes. And that leaves God one less explanatory gap to inhabit.
A current favorite refuge for those who deny that mutation and natural selection (also known as Darwinian evolution) are enough to explain the diversity of life on Earth is that highly-complicated biological structures cannot have been produced natrually. It’s basically a mouse-trap argument. A complicated structure such as, say, a receptor on a cell surface, is made of numerous components, just as a mouse trap is. No single component is of much use, just as the wooden base of a mouse trap is not much use without the bar and the spring and the other components. Since evolution confers survival only on useful components, continues the argument, it strains credulity to think that the individual parts of a receptor would have just coincidentally emerged from mutations at exactly the same time to come together in a useful structure. More likely, each component emerged, found nothing to do, and was eliminated by natural selection. Want a receptor? Ask God to make it.
Not so, say scientists who have determined, for the first time, how an ancient protein evolved step by step, refuting even more strongly a key element of the “intelligent design” argument.
In 2006 biologists reconstructed a receptor that last existed on earth 450 million years ago. Now the researchers have determined the structure of this recovered ancestor and figured out that specific mutations that, step by step, produced the modern-day glucocorticoid receptor, which allows cells to respond to the stress-hormone cortisol and therefore regulates stress. Says Joe Thornton, an evolutionary biologist at the University of Oregon who led both last year’s project and this one, “We were able to see the precise mechanisms by which evolution molded a tiny molecular machine at the atomic level, and to reconstruct the order of events by which history unfolded.” The study is being published today online in Science Express, the rapid-communication version of the journal Science.
The scientists found that just seven mutations changed the ancestral receptor gene into the gene that makes today’s glucocorticoid receptor. Some mutations would have wrecked the protein unless other mutations were in place first; this allowed the scientists to infer the sequence in which the mutations occurred. One crucial mutation resculpted a big section of the protein in a way that re-positioned a cluster of atoms; a second mutation in this region then tightened up the receptor’s embrace of cortisol. Other mutations buttressed other regions of the protein so they could withstand this remodeling. “Permissive mutations stabilized specific structural elements, allowing them to tolerate later destabilizing mutations that conferred a new function,” the authors write.
The result is “an unprecedentedly detailed view into the deep past of our genes,” Thornton told me. The discovery “provides the first fully mechanistic account of how a gene [for the ancestral receptor] evolved a new function [for the modern-day glucocorticoid receptor]. By comparing the ancestral structure to the modern structures that derived from it, we were able to see the mechanisms by which present-day receptors evolved.”
Thornton is not shy about his paper’s relevance to the unending evolution wars. The discovery, he says, “shows precisely how a complex phenotype evolved through a sequence of neutral and adaptive substitutions,” including those permissive mutations that do not themselves confer a selective advantage but pave the way for later mutations that do. A new book by the intelligent-design proponent Michael Behe argues that complex structures cannot evolve if they require two or more mutations. The new discovery shows that permissive mutations make this multi-step evolution perfectly possible—and in the case of the glucocorticoid receptor, a fact.