THE DEVELOPMENTAL GENETICS OF HYBRID INVIABILITY - A MITOTIC DEFECT IN DROSOPHILA HYBRIDS

We report studies of the developmental basis of hybrid inviability in the Drosophila melanogaster complex. The pathology of these hybrids cl osely resembles that of mitotic mutants in D. melanogaster. We use mos aic and cytological analyses to show that hybrid male inviability is a ssociated with, and probably caused by, a defect in mitotic cell divis ion. In the mosaic study, we find that male clones produced in otherwi se female hybrids are not cell lethal but are very small, probably ref lecting defects in mitotic proliferation. Cytological inspection of la rval neuroblasts reveals a profound mitotic defect in hybrids: chromos omes show a near-complete failure to condense even after 2 hr of incub ation in colchicine. Both the defect in clonal proliferation and in ch romatin condensation are rescued by mutations known to rescue normally inviable hybrid males. We present a simple model in which hybrid invi ability is partly or entirely caused by a mitotic defect; this defect is, in turn, caused by an interaction between the Hybrid male rescue ( Hmr) locus of D. melanogaster and autosomal gene(s) from D. melanogast er's sister species.