Allan Force

The Origin of Interspecific Genomic Incompatibility via Gene Duplication

One of the great unsolved mysteries of evolutionary biology concerns the genetic mechanisms underlying the origin of genomic incompatibilities between species. Two prevailing thoughts are that such incompatibilities often result from epistatically interacting genes that act as loss‐of‐function alleles in hybrid backgrounds or from chromosomal rearrangements that result in mis‐segregation during meiosis in hybrids. However, it is unclear how genes that cause a radical breakdown in hybrids arise without reducing fitness within species, and numerous cases of speciation appear to be unassociated with obvious chromosomal rearrangements. Here we suggest that duplicate genes, and more generally any kind of genomic redundancies, provide a powerful substrate for the origin of genomic incompatibilities in isolated populations. The divergent resolution of genomic redundancies, such that one population loses function from one copy while the second population loses function from a second copy at a different chromosomal location, leads to chromosomal repatterning such that gametes produced by hybrid individuals can be completely lacking in functional genes for a duplicate pair. Under this model, incompatibility factors accumulate with essentially no loss of fitness within populations as postulated under the Bateson‐Dobzhansky‐Muller (BDM) model of speciation and despite the fact that they arise from degenerative mutations. However, unlike the situation often envisioned under the BDM model, no change in the mode of gene action in hybrid backgrounds need be invoked. The plausibility of this model derives from a number of recent observations, including the fact that most genomes harbor substantial numbers of gene duplicates whose turnover is common and ongoing process and the fact that many genes have complex regulatory regions that facilitate their divergent resolution in sister taxa.

The zebrafish genome.

Publisher Summary Analysis of the zebrafish gene map suggests that during the course of vertebrate evolution, the zebrafish and human lineages have shared two rounds of whole genome duplication, and a third whole genome duplication event probably occurred before the teleost radiation. For many genes in humans, there may be two copies in zebrafish, and for many human chromosome segments, zebrafish is likely to have two such segments. The haploid zebrafish genome has 25 chromosomes, most of which are difficult to distinguish. These chromosomes contain about 1.7 X l0 9 base pairs of DNA, about half the mammalian genome size. The first genetic map of the zebrafish included about 400 genetic markers, mostly random amplified polymorphic DNAs (RAPDs), along with a few genes and mutations. The conservation of genome organization between humans and zebrafish can facilitate the transferal of information from one species to the other. The inference that zebrafish lineage appeared to have suffered an extra polyploidization step not experienced by mammals simply means that both zebrafish copies of a mammalian gene should be studied for better connectivity of molecular genetic mechanisms of development in zebrafish to the tetrapod—especially human—condition.

Larval regulation of adult longevity in a genetically-selected long-lived strain of Drosophila

Our previous work has shown that the major genes involved in the expression of the extended-longevity phenotype are located on the third chromosome. Furthermore, their expression is negatively and positively influenced by chromosomes 2 and 1, respectively. In this report we show that the expression of the extended-longevity phenotype is dependent on the larval environment. A controlled chromosome substitution experiment was carried out using a strain selected for long life (L) and its parent (R) strain. Twenty different combinations of the three major chromosomes were conducted and their longevities were determined under both high (HD) and low (LD) larval density conditions. The extended-longevity phenotype was only expressed under HD conditions. The chromosome interactions were not apparent under LD conditions. Density-shift experiments delineate a critical period for expression of the extended-longevity phenotype, extending from 60 h after egg laying (AEL) to 96 h AEL, during which the developing animal must be exposed to HD conditions if the extended-longevity phenotype is to be expressed. The change from HD to LD conditions is accompanied by statistically significant increases in body weight. The possible role of a dietary restriction phenomenon is examined and the implications of these findings discussed. It is now apparent, however, that the extended-longevity phenotype in Drosophila is a developmental genetic process.

Factors contributing to the plasticity of the extended longevity phenotypes of Drosophila

A number of laboratories have constructed independently derived long-lived strains of Drosophila, each of which have similar but not identical patterns of variability in their adult longevity. Given the observed plasticity of longevity within each of these strains, it would be useful to review the operational and environmental factors that give rise to this phenotypic plasticity and ascertain whether they are common or strain specific. Our review of the more extensively analyzed strains suggests that the allelic composition of the initial genomes and the selection/transgene strategy employed yield extended longevity strains with superficially similar phenotypes but which are probably each the result of different proximal genetic mechanisms. This then offers a plausible explanation for the differential effects of various environmental factors on each strains particular pattern of phenotypic plasticity. It also illustrates that the species has the potential to employ any one of a number of different proximal mechanisms, each of which give rise to a similar longevity phenotype.