In other words it explains extinctions, but not survival
Well, the literal
dilemma refers to the problem for the population, not individual survival, yes. People have--mistakenly--come to think of "Haldane's Dilemma' as a dilemma for evolutionary theory, which it definitely is not.
But it is not restrictive on other populations. It does not affect short generation populations, nor does it affect the survival of long generation populations outside the area of stress, which can then later radiate back into an extinction evacuated niche.
Given that this is the pattern of evolution that we actually see following extinction events, this is no surprise either.
No, it isn't. However, it is important to keep in mind that there is a cost associated with any gene substitution, so Haldane's work can be applied generally, even though it's true that the basic assumptions of his model in the original papers were somewhat restrictive. Let's take a look at each:
1.
Large, randomly mating population. This should not be controversial-- it's very common in population genetics models. Haldane was interested in the effects of selection, so he assumes a large population to eliminate any stochastic effects of genetic drift on the analysis. Of course (and Haldane was very aware of this) in
any finite population genetic drift does play a role.
2.
Constant population size. Again, this shouldn't be controversial. What was interesting to Haldane (and other population geneticists such as Crow and Kimura) was the common observation that substitutions could go on and populations would not change much in size.
3.
The allele starts in the population at a very low frequency. Haldane had in mind an allele that was originally harmful, and kept in the population purely by mutation pressure, but which became beneficial when the environment suddenly and drastically changed for the worse. Nothing particularly unusual with that, though (as we will see later) the higher the initial frequency of a beneficial allele, the lower the cost of substitution. If it sounds odd that a beneficial allele could
begin at a high frequency, consider an allele that is originally neutral, rising to a high initial frequency due to drift,
then becoming selected for when the environment changes, and I think you can see one way such a thing can come to pass.
Haldane also made a couple of other minor assumptions in the initial paper (such as constant selective value throughout the substitution), but we won't get into those since they don't have much to do with the "controversy".
Haldane's key insight here wasn't that, on average, a population could only endure 1 substitution per 300 generations, as many seem to think. Instead, what made Haldane's paper so interesting was his revelation that, as long as selection wasn't intense, the
cost of substitution was independent of selective value. Instead, the cost was entirely dependent on the allele's frequency in the population when selection for it began. This makes sense if one thinks carefully about what is happening with the substitution of one allele for another: the beneficial allele must have some kind of reproductive advantage over its rival. In some way it must be making more copies of itself at the expense of the other. Natural selection can favor an allele by simply enabling it to have greater reproductive capacity over another”it doesn’t have to be a case of killing off individuals who carry the rival allele (that would be the case of intense selection that Haldane pointed out was an exception to his model). But, ultimately, it comes down to one allele having enough reproductive excess over the other to eventually replace it. With this in mind, it should now be very clear why the initial frequency is so important: it determines what frequency of the population must be replaced with individuals carrying the new allele, and therefore how long that will take.
Haldane originally used genetic death (juvenile mortality or its equivalent in reduced fertility) as the currency to measure the cost of substitution. Remine prefers to use pure reproductive excess in his book and paper, but in reality they are ways of measuring the same thing. Many authors on the subject (Warren Ewens, Joe Felsenstein, James Crow, Motoo Kimura, and Masatoshi Nei) clearly understood that reproductive excess is the heart of the discussion, and said so clearly in their papers in the late 60’s and early 70’s. I know Remine thinks his approach is cleaner, and I agree, from what I’ve seen of his work. But I disagree with his insistence that the others were confused or that his approach is so radically different. It must have been galling when both Ewens and Crow, who reviewed his paper when he submitted it to
The Journal of Theoretical Biology, said he wasn’t really saying anything that they hadn’t already been saying since the 60’s, but it’s true. So it should come as no surprise that neither of them recommended publication in that particular journal, since it does not contribute significantly new theory. Remine likes to complain that he is being suppressed, but Crow has publicly made it clear he thinks Remine’s paper could be published in another journal. I think so as well, though I must say, after reading it, that Remine clearly has no idea how to write a scientific paper. Its style is so poor it is surprising that Remine spent such a long time wrangling with editors and reviewers not only with the
The Journal of Theoretical Biology but with
Heredity as well. One would have thought he could have taken their input or at the very least look at some articles in them and modified his manuscript. Looking at what he eventually published online, it’s obvious he did neither.
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