Specific questions regarding general rules in organismic biology can sometimes be rather tricky to answer…because of variation between taxa and environmental context there are usually exceptions. A visitor to this website had a few questions regarding asymmetry and heterozygosity, and I responded that the relationship between the two (generally assumed to be a negative one, that is, heterozygosity tends to correlate with less asymmetry) is one where the latter influences the buffering of the developmental arc which leads to bilateral symmetry. When you see lists of traits with heritabilities bilateral symmetry tends to show a low heritability. The reason is that it is usually considered a genetic trait, there is strong selection against any mutations which would result in asymmetries because such a phenotype is not very fit. That being said, perfect symmetry is not achieved because there are other factors which affect the developmental arc of an organism, whether they be environmental or genetic. I offered that the relationship between heterozygosity and lower fluctuating asymmetry results from the more robust immune systems of heterozygous individuals. The logic is that infection tends to interfere with optimal development. Obviously this logic is most relevant in the case of organisms with adaptive immune systems, so I’m not going to point to flie studies. Here is an on point quote from Asymmetry, Developmental Stability, and Evolution
The clear relationships between parasitism and disease and asymmetry may have environmental or genetic origins (Thornill and Moller 1997). The genetics of disease susceptibility in relation to developmental instability have been investigated to some extent for humans by Russian geneticists. Botvinev et al. (1980) found that children with non-modal [rare] body mass suffered disproportionaly from a range of diseases including infectious diseases. These groups of children were characterized by deviant allele frequencies for blood group loci and lower levels of heterozygosity. Althukov et al. (1981) noted that children with acute pneumonia have a marked disposition to viro-bacterial diseases, a high frequency of small developmental anomalies, and a smaller body length and mass at birth. The study also demonstrated significant differences in four genetic systems between the two groups of children, a lower heterozygosity per locus, and a higher frequency of rare antigen combinations and rare electrophoretic protein variants….
More study needs to be done of course (I emailed a researcher who has done some relevant studies, but they seem unpublished for now). Heterozyogsity is not the only variable affecting symmetry and developmental stability (rare alleles probably alludes to deleterious mutations, though heterozygosity is related to this because of its masking potential). There are studies which show that lines of flies that have been separated for many generations may give rise to hybrids which are less developmentally stable. This is not due to a less robust immune system (flies don’t haven’t adaptive immune systems), but likely there are coadapted gene complexes which have evolved in diverging genetic backgrounds and the F1 generation exhibit deleterious epistatic effects.1 Speciation is probably one end outcome of this process as hybrids eventually become inviable.
Related: Here is the PUBMED query for “developmental stability heterozygosity.”
1 – Imagine an ancestral population with genotype AABB. In population 1 there might a mutation which gets fixed so that the population is now AAbb. Now imagine a second substitution so that population 1 is now aabb (the BB -> bb substitution happened first!). Assume that population 2 remains AABB. If there were epistatic interactions between the two loci, then an AaBb genotype might be less fit because of negative epistatic effects between the ancestral and derived states.
Posted by razib at 02:50 PM