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.