Sexual Recombination

By Branden Holmes (Surroundx) on November 28, 2010

“In one sense, we are all equally old, about four billion years, that is, as old as life itself. The difference between an individual who is sixty years old and one who is twenty is how far back into the past their unique genotypes extend. The genes inside a twenty-year-old have survived just as long as those in a sixty-year-old. It is just that in the twenty-year-old the genes were united just 21 years ago, from two separate individuals, each conjoined with other genes. In short, they have undergone recombination more recently than have the genes of the sixty-year-old.” (Robert Trivers, Natural Selection and Social Theory, pg. 241) Even without considering mutations, there is much variation that can created through sexual recombination: the shuffling of genes from two parents into one child’s DNA. Of course, this takes a large number of heterozygous genes (numerically not proportionally) as an assumption. But because genes only code for proteins and not traits directly, different combinations of proteins will produce slightly different phenotypes, while still retaining a general and recognizable phenotype unique to that species (excepting cryptic species). For this reason, we are not averages of our parents.

Without even considering mutations some individuals may be coincidentally immune to a particular disease or coincidentally (to all intents and purposes) better adapted to survive than others. The resistance to the disease myxamatosis by rabbits almost certainly occurred as a result of sexual recombination, which explains why less than one percent of the original population of both outbreaks survived the deliberate outbreaks. If the resistance was caused by having a particular allele of a particular gene, then we would have expected to see a dramatic decline in the number of rabbits killed the second time around that the disease was deliberately released. Eventually most rabbits “acquired” immunity from the disease because the population went through a bottle-neck, which, as a matter of necessity means a decline in variation because all of the individuals carrying any given recent mutation were likely to have perished because of the sheer disproportionate death rate during the selective events that we recognize as the release of the myxamatosis disease. (paragraph). Sexual recombination serves a vital purpose other than creating variation within a population: it prevents inbreeding in sexually reproducing species. Asexually reproducing don’t suffer from it because of their limited genomes, and even some sexually reproducing animals don’t seem to be affected such as reptiles, parthenogenic species, and asexually reproducing animals who have evolved from sexually reproducing ones. Sexual recombination helps to prevent too many homogenous genes which cause serious birth defects, which increases infant mortality rates and hence a domino effect until the species or population becomes extinct. (paragraph). Mutations are constantly "fighting" for fixation while the "aim" of sexual recombination is in a sense to prevent fixation. The way in which this is accomplished is that each individual is a different combination of genes, and so if one combination (an individual) dies, there are other combinations with that particular gene, which, because they are all different combinations are not likely to fall victim to the same selective event, whatever that may be. In given successful gene can expect to find itself in the bodies of many individuals of a wide range of "fitness" levels. If that gene is beneficial to its possessors, it will on average expect to find itself inside an individual which reproduces and passes on that gene. Of course not all individuals with that gene will survive to maturity, or even most, because each of those combinations is of inferior phenotypic cohesion. (paragraph). In light of this we realise that adaptation does not necessarily involve new mutations. It may simply be that natural selection selects from the variation that is already there. There is enough contemporary variation within a populations gene pool to withstand most selective events, partly because there has to be. Species cannot wait around for the right mutations to occur because the probability of that occurring is miniscule. And as we have seen from the chapter on natural selection, all selective events merely select between already existent alleles (in most if not all cases only one or a few). Selective events fast track fixation of genes, but because they are very selective in nature, only concerned with one or a few genes, many different selective events are required for any great amount of evolutionary change to be brought about in a single species. (paragraph).

Related articles:
adaptation, Evolution, gene

About Branden Holmes
I am an amateur evolutionist interested in the theoretical side of the subject.

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