Testing the Drosophila maternal haploid gene for functional divergence and a role in hybrid incompatibility

Crosses between Drosophila simulans females and Drosophila melanogaster males produce viable F1 sons and poorly viable F1 daughters. Unlike most hybrid incompatibilities, this hybrid incompatibility violates Haldane’s rule, the observation that incompatibilities preferentially affect the heterogametic sex. Furthermore, it has a different genetic basis than hybrid lethality in the reciprocal cross, with the causal allele in Drosophila melanogaster being a large species-specific block of complex satellite DNA on its X chromosome known as the 359-bp satellite, rather than a protein-coding locus. The causal allele(s) in Drosophila simulans are unknown but likely involve maternally expressed genes or factors since the F1 females die during early embryogenesis. The maternal haploid (mh) gene is an intriguing candidate because it is expressed maternally and its protein product localizes to the 359-bp repeat. We found that this gene has diverged extensively between Drosophila melanogaster and Drosophila simulans. This observation led to the hypothesis that Drosophila melanogaster mh may have coevolved with the 359-bp repeat and that hybrid incompatibility thus results from the absence of a coevolved mh allele in Drosophila simulans. We tested for the functional divergence of mh by creating matched transformants of Drosophila melanogaster and Drosophila simulans orthologs in both Drosophila melanogaster and Drosophila simulans strains. Surprisingly, we find that Drosophila simulans mh fully complements the female sterile phenotype of Drosophila melanogaster mh mutations. Contrary to our hypothesis, we find no evidence that adding a Drosophila melanogaster mh gene to Drosophila simulans increases hybrid viability

TESTING THE ROLE OF D. MELANOGASTER MATERNAL HAPLOID IN A D. SIMULANS X D. MELANOGASTER HYBRID CROSS

Hybrid incompatibility (HI) (such as hybrid sterility or lethality) is a reproductive isolation barrier that contributes to speciation. Genes have been identified whose interaction causes HI; however, identifying the factors (i.e. maternal genes, small RNAs, etc.). HI is essential to understanding how these genes function to affect hybrid development. Previous studies have shown that when D. melanogaster female parents are mated with D. simulans male parents, the interaction of two genes - Hybrid male rescue and Lethal hybrid rescue - causes hybrid male lethality. When a D. simulans female parent is crossed with a D. melanogaster male parent we observe the opposite outcome: hybrid female offspring die in the embryo stage while hybrid males live. At this stage, embryonic cells fail to undergo mitosis appropriately. During anaphase, the X chromatids segregate partially or not at all. This abnormal segregation is attributed to the 359-bp satellite DNA in D. melanogaster which maps to the Zygote hybrid rescue (Zhr) locus. Since we know that in a pure D. melanogaster cross, all of the offspring live, we hypothesize that there is a factor which regulates Zhr to allow for normal mitosis to occur. Maternal haploid (Mh) is maternal factor which is an important protease involved in decondensation of the paternal genome during zygote formation. To test whether maternal haploid is a potential factor which drives HI, we created transgenic strains of D. simulans which contained the D. melanogaster maternal haploid protease. I then mated female transgenic flies with D. melanogaster males and compared the hybrid progeny results to that of the control cross. I found that with the presence of D. melanogaster maternal haploid in the genome of the D. simulans fly, the female hybrid viability rate was higher than among the female hybrid progeny of normal D. simulans flies. This shows that maternal haploid is a factor that contributes to hybrid viability