James Plaskett has been directing us to the anti-Darwinian writings of Richard Milton in support of the claim that there are no spontaneous beneficial mutations.
The go-to experiment for beneficial mutations is undoubtedly the very long and painstaking work led by Richard Lenski, which showed the spontaneous appearance of bacterial lines able to metabolise citrate. These are generations raised in over twenty years of research in which samples are frozen, where the appearance of a mutation can be demonstrated to arise and arise repeatedly, and these mutations are not merely the ready re-expression of a formerly dormant capacity.
But I don’t think Milton was aware of that instance when he wrote. Then, the classic case was antibiotic resistance in bacteria:
“For instance, from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance. In this case (in contrast to the situation with the peppered moth populations described above) origin of the population from a single bacterium allows comparisons of the mutated genes with the corresponding genes from the original bacterium, verifying that the variant sequences were not present before the culture with antibiotics and therefore arose as de novo beneficial mutations.”
Edward Max, http://www.talkorigins.org/faqs/fitness/ 1.2.1
Let’s turn to Milton’s objections (which have fallen off the web, but I presume Milton still stands by them):
“This claim can never be strictly true. In order to do what Dr Max describes here, the experimenter would necessarily have to both culture the new population from his single experimental bacterium AND fully sequence the DNA in that same single bacterium for later comparison. But, of course, analysing the DNA of the experimental bacterium must necessarily destroy it, making it impossible to culture from.
“Instead the experimenters do the next best thing: they select a number of individuals from the same culture, which they assume to be genetically identical and they analyse the genes of one (or more) and use the others to culture the new colony. If the bacterium they select to analyse appears not to have any genes for antibiotic resistance then they assume that the same must be true for its close relative they are using to breed.”
I think that ‘genetically identical’ assumption is a good one, and can also be shown to be true. Because these are bacteria arising from asexual reproduction of a single cell (a routine microbiological technique), they are all necessarily genetically identical ‘twins’ and will remain so until the appearance of any mutations. You can sample from the population to show that whatever it takes to be resistant to an antibiotic is not there at one point and is there at a later point.
You can even see this in real time. A bacterial population with a single founder will spread across a plate up a gradient of increasing antibiotic concentration until they are brought to a halt by the antibiotic. After a pause, suddenly and spontaneously, they break through to the neighbouring area of the plate which was previously uninhabitable. (I seem to remember seeing that on Bang Goes The Theory earlier this year.)
“Despite Dr Max’s denials, the case of antibiotic resistance in microorganisms is exactly the same in principle as that of so called ‘industrial melanism’ in the peppered moth. It is simply a case of one variety of the species flourishing while another variety dies off, because of changed environmental conditions.”
I think that shows that Milton hasn’t understood the power of the single-founder experiments. There is only one variety to start with.
“…It is perfectly feasible that many bacteria possess genes that can provide resistance — whether or not those genes are currently expressed, and whether or not they have even been identified by geneticists as genes for providing antibiotic protection. Such unexpressed genes are known to be sometimes ‘switched on’ by environmental pressures of just the life-threatening kind that are applied to bacteria in the lab. So, even if antibiotic resistance were genuinely arising during the experiment, it is not necessarily arising de novo, as Dr Max claims, but may merely be a genetic throwback.”
It may be the work hasn’t been done to exclude this possibility in every case, but certainly there are many examples of single changes in DNA sequences that produce antibiotic resistance. These cases are not due to the turning on of an unexpressed pre-existing capacity, these are spontaneous beneficial mutations in a gene expressed throughout (http://aac.asm.org/content/44/7/1771.full).
The Lenski team has also nailed what is going on in their experiments, and it too is certainly not the recovery of a previously unexpressed capacity.
Milton also offers:
“Perhaps Dr Max and other convinced Darwinists might say that choosing one bacterium for genetic analysis and a very close relative for culturing is as close as one can get to experimental certainty, and is almost scientific proof. But the whole point of science is that ‘almost’ isn’t good enough.”
Although I think the lab work is immune to the criticisms Milton offers, I think this statement is also worth challenging: it is a misconception about the nature of science. As close as you can get to certainty is as close as you can get, and if you demand a higher standard, you are demanding, not just proof beyond reasonable doubt, but proof beyond unreasonable doubt. And that’s Milton’s problem, not a problem with the neo-Darwinian synthesis.
Reflection: It’s actually enough for only one element of the neo-Darwinian synthesis to fail: for mutations to be too uncommon or never beneficial, or for natural selection never to be observed in or out of the lab., nor mating barriers; or for the molecular tree to contradict the morphological tree, or for some other prediction to be disproved… And yet it seems Milton wishes to dispute every little bit of it. He protests too much.