Razib Khan One-stop-shopping for all of my content

July 27, 2010

Snap, phenotype, genotype and fitness





There are various ways one presumes that hybrid vigor could emerge. One the one hand the parental lines may be a bit too inbred and therefore have a heavier than ideal load of deleterious alleles which express recessively. Since two lineages will likely have different deleterious alleles, crossing them will result in immediate complementation and masking of the deleterious alleles in heterozygote state. Another model is that two different alleles when combined in heterozygote state have a synergistic fitness effect. We generally know of heterozygote advantage in cases where there’s balancing selection, so that one of the homozygotes is actually far less fit than the other, but the fitness of the heterozygote is superior to both homozygotes. But that is not a necessity, and presumably there could be cases where both homozygotes are of equal fitness, but the heterozygote is of marginally greater fitness.

As for hybrid inferiority, a simple model for that is that lineages have co-adapted complexes of genes which are enmeshed in gene-gene networks. These networks are finely tuned by evolution and introduction of novel alleles from alien lineages may lead in destabilization of the sensitive web of interconnections. This model taken to an extreme is a scenario whereby speciation could occur if two lineages become mutually exclusive on a particular genetic complex which is “mission critical” to biological machinery (imagine that the gene involved in spermatogenesis is effected).

These stories are fine as it goes, but they do have something of an excessively ad hoc aspect. A little light on formalization and heavy on exposition. In this paper the authors aim to fix that problem. To explore genetic interactions in hybrids, and how they effect gene expression, they selected the genus Antirrhinum as their model. These are also known as “snapdragons.” Like many plants Antirrhinum species can hybridize rather easily across species barriers. They observe the effect of taking genes from a set of species and placing them in the genetic background of another. In particular they are focusing on A. majus, hybridizing it with a variety of other Antirrhinum species, as well as introgressing alleles from the other species onto a A. majus genetic background (so an allele on a specific gene is placed within the genome of A. majus).

Just as they focus on a specific genus of organism, so they also focus on a specific set of genes and the molecular and developmental genetic phenomenon associated with those genes. The genes are CYC and RAD, which are located near each other genomically, with CYC being a cis-acting regulator of RAD. In other words, CYC modulates the expression of RAD which is on the same chromosome.  Variance in gene expression simply defines the concrete difference in levels of protein product. Mutant variants of CYC and RAD, cyc and rad, are created by insertion of transposons. Insertion of transposons can abolish gene expression, resulting in removal or alteration of function. What is that function? I’m rather weak on botanical morphology, so I’m going to be cursory on this particular issue lest a reader correct me strenuously for misapplication of terminology. So I’ll show you a figure:


I added the labels. C is basically what majus should look like, while G is a totally “ventralized” mutant. B and F approach wild type, but the other outcomes are more mixed. Note the genotypes in the small print. Table 1 measures the expression levels of the gene product for the various genotype:

journal.pbio.1000429.t001 (1)

Look at the first row; mutant variants of CYC which are nonfunctional reduce normal copies of RAD down to 20% levels of gene expression. That’s because CYC is a transcriptional regulator of RAD. The process is not reversed. RAD lacking functionality does not impact CYC (last row). Finally, the heterozygote states does result in reduced dosage of the gene product. Though the phenotypes might be closer to wild type than the mutant, the molecular expression of the gene is substantially changed. This is one of the issues which is always important to remember: the extent of dominance exhibited by a sequence of phenotypes consequent from a particular genotype may vary dependent on which phenotype you are a highlighting. On a molecular level there is incomplete dominance. Additive effects. On the level of exterior morphology there is more perceived dominance. This is not even addressing the issue of pleiotropy, where the same gene may have dominant and recessive expression on two different traits simultaneously in inverted directions (i.e., the recessively expressed allele in trait A may be dominant in B, and vice versa).

Figure 1 shows the different allelic expression levels in hybrids of Antirrhinum species. But what about the impact of the combinations on phenotype? I’ve reedited figure 4 so it fits better on this page:


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