Genetic Polymorphism Quotes

Genes have plenty to do with behavior. Even more appropriately, all behavioral traits are affected to some degree by genetic variability.65 They have to be, given that they specify the structure of all the proteins pertinent to every neurotransmitter, hormone, receptor, etc. that there is. And they have plenty to do with individual differences in behavior, given the large percentage of genes that are polymorphic, coming in different flavors. But their effects are supremely context dependent.

In Darwin's time no serious attempt had been made to examine the manifestations of variability. A vast assemblage of miscellaneous facts could formerly be adduced as seemingly comparable illustrations of the phenomenon "Variation." Time has shown this mass of evidence to be capable of analysis. When first promulgated it produced the impression that variability was a phenomenon generally distributed amongst living things in such a way that the specific divisions must be arbitrary. When this variability is sorted out, and is seen to be in part a result of hybridisation, in part a consequence of the persistence of hybrids by parthenogenetic reproduction, a polymorphism due to the continued presence of individuals representing various combinations of Mendelian allelomorphs, partly also the transient effect of alteration in external circumstances, we see how cautious we must be in drawing inferences as to the indefiniteness of specific limits from a bare knowledge that intermediates exist.

The creation of new symbioses by mergers on a crowded planet is called symbiogenesis. And we might call all aspects of its study “symbiogenetics”—the science of normative symbioses, the word commanding respect because of its apparent coinage from genetics; in fact, I derived it directly from symbiogenesis, though the connotation is a good one. Although this type of evolution sounds bizarre—a monstrous breach of Platonic etiquette in favor of polymorphous perversity—it is now confirmed by genetic evidence, taught in textbooks. It is a fact, or what the French philosopher of science Bruno Latour and the Belgian physicist-turned-philosopher Isabelle Stengers, not putting too fine a point on it, would call a factish. Nonetheless, although symbiogenesis—the evolution of new species by symbiosis—is now recognized, it is still treated as marginal, applicable to our remote ancestors but not relevant to present-day core evolutionary processes. This is debatable. We are crisscrossed and cohabited by stranger beings, intimate visitors who affect our behavior, appreciate our warmth, and are in no rush to leave. Like all visible life-forms, we are composites.

With the rise of molecular genetics, it has become possible to search for possible changes (mutations, polymorphisms) in target genes. Much effort has gone into investigating variations in genes that contribute to serotonin transmission, because serotonin-related drugs have antidepressant and anxiolytic properties. This assumes, however, that the treatment mechanism is the same mechanism that gives rise to the disorder.53 Although this is consistent with the old chemical imbalance hypothesis, it is not a conclusion that should simply be accepted without careful assessment. Nevertheless, studies of the genetic control of serotonin have found interesting results. For example, people with a certain variant (polymorphism) of a gene controlling a protein involved in serotonin transmission are more reactive to threatening stimuli, and this hyperreactivity is associated with increased amygdala activity during the threat.54 Further, it has been reported that this variant of the gene can account for 7 percent to 9 percent of the inheritance of anxiety.55

Modeling the evolution of modularity became significantly easier after a kind of genetic variation was discovered by quantitative trait locus (QTL) mapping in the lab of James Cheverud at Washington University called 'relationship QTL' or r-QTL for short. An r-QTL is a genetic locus that affects the correlations between two quantitative traits (i.e. their variational relationship, and therefore, 'relationship' loci). Surprisingly, a large fraction of these so-mapped loci are also neutral with respect to the character mean. This means one can select on these 'neutral' r-QTLs without simultaneously changing the character mean in a certain way. It was easy to show that differential directional selection on a character could easily lead a decrease in genetic correlation between characters. Of course, it is not guaranteed that each and every population has the right kind of r-QTL polymorphisms, nor is it yet clear what kind of genetic architecture allows for the existence of an r-QTL. Nevertheless, these findings make it plausible that differential directional selection can enhance the genetic/variational individuality of traits and, thus, may play a role in the origin of evolutionary novelties by selecting for variational individuality. It must be added, though, that there has been relatively little research in this area and that we will need to see more to determine whether we understand what is going on here, if anything. In particular, one difficulty is the mathematical modeling of gene interaction (epistasis), because the details of an epistasis model determine the outcome of the evolution by natural selection. One result shows that natural selection increases or decreases mutational variance, depending on whether the average epistatic effects are positive or negative. This means that the genetic architecture is more determined by the genetic architecture that we start with than by the nature of the selection forces that act upon it. In other words, the evolution of a genetic architecture could be arbitrary with respect to selection.

Sequences of base pairs, called genes, code for and produce gene products such as proteins. If just one of the base pairs is altered by mutation, say from ultraviolet damage, a virus, or cigarette smoke, the resulting protein will be aberrant, and usually faulty. Some of these mutations are not fatal and are actually kept by the cells and the population. These are called single nucleotide polymorphisms, or SNPs. If the incidence of the change is found in less than 1 percent of the population of humans, it is called a mutation; if more than 1 percent, it is typically called an SNP. There are about twenty million SNPs found in humans, and they account for many differences in the appearance and behavior of people, from curly hair to obesity to drug addiction. It is these SNPs where the hunt for genetic “causes” of traits and diseases has focused since the 1990s.