Characterization of defects in adult germline development and oogenesis of sterile and rescued female hybrids in crosses between Drosophila simulans and Drosophila melanogaster. H. Hollocher 1, K. Agopian 2, J. Waterbury 2, R.W. O'Neill 1, A.W. Davis 3. 1) Ecology & Evolutionary Biology, Princeton University, Princeton, NJ; 2) Department of Molecular Biology, Princeton University, Princeton, NJ; 3) Department of Biological Sciences, Webster University, St. Louis, MO.
A remarkable and often repeated pattern when crossing different species is the tendency for interspecific hybrids to be completely sterile. The profound disturbances found in the gonads of hybrids contrasts sharply with the normality of the soma. Although degeneration of the gonads in interspecifc hybrids has long been well known, the molecular and developmental genetic causes of this phenomenon are not well understood. Crosses between Drosophila melanogaster and D. simulans normally result in progeny that are either inviable or sterile. Recent discovery of strains that rescue these inviability and sterility phenotypes have made it possible to study the developmental basis of reproductive isolation between these two species in greater detail. Through examination of the protein product staining patterns of genes involved in early germline development and gametogenesis, we have found that hybrid female sterility results from the improper control of mitotic cell divisions involved in primordial germline proliferation, germline stem cell maintenance, and cystoblast formation and differentiation during early oogenesis. Rescued hybrid females are fertile, yet they have lower amounts of adult germline from the onset and show a premature degeneration of adult germline stem cells with age. In addition, older rescued hybrid females also exhibit mutant egg phenotypes associated with defects in dorso-ventral patterning. Hybrid males from these same crosses have no detectable germline in adult reproductive tissues, even when hybrid sterility rescue strains are used. These germline and gametogenic defects are discussed in light of what is known about the evolution of hybrid inviability and sterility.