From the archives comes this bit about the ludicrous (and willful) misunderstanding that creationists have regarding ‘beneficial’ mutations:

Whether they are young earthers or intelligent design advocates, one tactic creationists use is to claim evolutionary biologists-always described as “evolutionists”-think something which we do not. Over at Thoughts from Kansas, Josh had a very nice post describing the mechanisms by which mutations happen (among other things). Without fail, in charged a creationist:

The evolutionists make the claim that there are enough mutations that turn out to be beneficial to account for our present level of development.

Let’s forget for a moment this statement is so vague and imprecise as to be impossible to substantiate with any form of evidence. And let’s also forget the implicit idiocy underlying that statement: that all of the ‘beneficial’ mutations showed up at once (which would be very difficult to imagine), as opposed to resulting from millions (or billions, depending on how far back you want to go) of years of ongoing evolution.

What really bothered me is the misuse of “beneficial”: that’s where all of the IDiocy starts. This creationist doesn’t seem to understand is that yesterday’s variable gene that has ‘beneficial’ variants or alleles often becomes today’s invariant (or mostly invariant) gene. I’ve given you the punchline, so now we’ll walk through this.

Imagine a gene has two alleles that we’ll call “A” and “a.” Let’s assume that A is beneficial, that is, it confers a fitness increase. Furthermore, this fitness increase due to A is universal: it applies everywhere, and in all environments*. This advantage could be anything: maybe it’s easier to squeeze offspring through the birth canal, maybe it’s a new, improved kind of tooth, an immune system that can now recognize a virus, or anything else you can imagine. When allele A initially evolves, it is rare (obviously, when it arises, there is only one copy of it in the entire population). Because it is beneficial, its frequency will rise, and A will ultimately predominate the population (note: this is an oversimplification).

Here’s the rub: once A becomes predominant, “a”, the ‘nonbeneficial’ allele will vanish (once “a” becomes very rare, it will eventually disappear by random chance). Thus, what was a gene with variation which allowed you to discern a ‘beneficial’ allele is now a gene with no variation that doesn’t appear to be beneficial.

This might seem tautological. However, there are cases where we can observe beneficial alleles. One case is when the ‘selective sweep’, the increase of A, is ongoing. One such instance is antibiotic resistance in bacteria; another is pesticide resistance in crop pest insects. The other way we can observed beneficial alleles is during balancing selection.

Balancing selection occurs when the two forms of the gene are advantageous under different ecological conditions. For example, toxic metal resistant plants are favored in pollution heavy environments, whereas the ‘normal’ form is found in non-polluted habitats. Balancing selection implies that there are tradeoffs between the two forms. It also requires that there are ecological conditions that maintain these tradeoffs: if the environment changes such that balancing selection no longer operates (e.g., the pollution is cleaned up), then bye-bye balancing selection.

So beneficial mutations will be hard to observe for two reasons. First, the universally beneficial alleles will be difficult to spot because the non-beneficial variation will have been removed by natural selection. Second, most cases where we can identify beneficial mutations, these mutations will not be universally adaptive. While this makes them easy to identify, these won’t be that common because the right mix of environmental properties is needed. Many genes where we can identify differences in fitness will resemble pesticide resistance, where the fitness advantage is contingent on the environment.

The good news is that while identifying beneficial mutations experimentally can be difficult (or where there’s no variation, impossible), we can identify the “ghost of selection past” using DNA sequence. But that will have to be the subject of another post.

*and in all genetic backgrounds too. The fitness effect of a given allele often depends on what other genes it occurs with (epistasis).

A couple of general points: To the biologists, yes, this is a simplification (hopefully, not an oversimplification). To everyone, I’ve kept the situation simple: two alleles. In natural populations, there may be dozens (or even more). In my own work, when I look at ~100 different isolates of E. coli, I usually find ~40-50 alleles. Much of the variation, however, doesn’t change the protein structure, and is known as ‘silent’ (if you know what codon bias is, bully for you. So do I. Now stow it). Many of the DNA variants that result in protein changes also don’t appear to do much (although some protein changes have considerable effects-like everything else in biology, it depends)