Abstract
Crosses between Drosophila melanogaster females and D. simulans males produce viable hybrid females, while males are lethal. These males are rescued if they carry the D. simulans Lhr gene. This paper reports that females of the wild-type D. melanogaster population Staket do not produce viable hybrid males when crossed with D. simulans Lhr males, a phenomenon which we designate as the Staket phenotype. The agent responsible for this phenomenon was found to be the Staket X chromosome (Xmel, Stk). Analysis of the Staket phenotype showed that it is suppressed by extra copies of D. melanogaster rDNA genes and that the Xmel, Stk chromosome manifests a weak bobbed phenotype in D. melanogaster Xmel, Stk/0 males. The numbers of functional rDNA genes in Xmel, Stk and Xmel, y w (control) chromosomes were found not to differ significantly. Thus a reduction in rDNA gene number cannot account for the weak bobbed Xmel, Stk phenotype let alone the Staket phenotype. The rRNA precursor molecules transcribed from the Xmel, Stk rDNA genes seem to be correctly processed in both intraspecific (melanogaster) and interspecific (melanogaster-simulans) conditions. It is therefore suggested that the Xmel, Stk rDNA genes are inefficiently transcribed in the melanogaster-simulans hybrids.
