Robert T. answered • 09/26/19
Masters degree in biology with 4 years of teaching experience
They don't, but we are lead to think that they do. Remember, evolution is blind -- good or bad alleles are just points of view, many of which that are determined by natural selection (or other forms of selection, such as breeding or sexual selection). The most common fate for a random mutation is a random gene is that it will have no effect on fitness. The next assumption is that most mutations are recessive. Of course, there are plenty of examples of dominant mutations, but those are under stronger selection, typically, and if they are detrimental, do not persist long in a population as just the one copy reduces fitness, at best, or is outright lethal, at worst. The point is: most mutations are neutral and are recessive. If they turn out to be "bad" mutations, they can persist in a population for a very long time at very low frequency, because having one bad allele isn't detrimental. However, in a small population size, the probability of mating with somebody with a recessive allele increases; this is why small, isolated populations tend to be less fecund, more susceptible to disease, and/or harbor diseases that are "characteristic" of their group, such as Tay Sachs disease in some Jewish populations. In humans, incest is almost always a willful act -- that is, it's not blind or random, but actually a form of selection. Families that decide to marry only within the family, or with closely related cadet branches of the family, are selecting for closeness in relatedness. So, in those cases, it's really no different than a small breeding population.
As you alluded, it is possible for "bad genes" to have other functions that may be beneficial, and your absolutely correct in that statement. If you were to get into microbiology, immunology, or virology, there will be lots of talk about how such and such host cell has a "viral receptor" for, say, HIV or chicken pox, or whatever. It too got me thinking "why would a host evolve susceptibility to a deadly virus?" and the answer, again, is "they didn't". Rather, the virus evolved to use that particular host marking (it can be a receptors, a protein, a carbohydrate, anything really) that is so important for the host that mutating it to be unusefull to the virus is more costly (ie deadly) to the host. To go back to HIV, HIV uses a receptor found on T-helper cells called CCR5. This receptor is very important for immune function, so deadly mutations are quickly removed from teh population. That being said, there are rare people who have small mutations (a deletion, actually) in this gene that encodes this protein, that just so happens to be the part that the HIV needs to bind to and infect the cell.
Your last point, about benefits of inbreeding are true. I don't remember the term for it, but if you have an incestuous population, initially, they have reduced fitness. But once you weed out all those bad alleles, you may actually improve fitness. Though not for that purpose, this is done in research animals; I work with mice, and many mouse lines are so imbred that they are basically clones. This would be a terrible t hing in the wild -- if one animal got sick, the entire colony would collapse -- but this is not so in captivity, where we can control their entire environment. Having a super incestuous rodent population is useful because you can basically rule out genetic variability between experimental and control groups as an explanation for some phenomenon.
