Ontogenetic consequences of dysgenic crosses in Drosophila virilis
Original Article | Published: 13 December 2013
Marina I. Sokolova1, Elena S. Zelentsova1, Natalia G. Shostak1,
Nikolay V. Rozhkov3 and Michael B. Evgen’ev*1,2
1Engelhardt Institute of Molecular Biology, Moscow, Russia, 2Institute of Cell Biophysics, RAS, Pushchino, Moscow region, Russia and 3Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA
ybrid dysgenesis (HD) syndrome in Drosophila virilis presumably results from the mobilization of several unrelated mobile genetic elements in dysgenic hybrids. Morphogenetic events during oogenesis and spermatogenesis were investigated in detail in the progeny of D. virilis dysgenic crosses. Using germ-cell specific anti-Vasa staining, we monitored the fate of germline cells at different ontogenetic stages in strains of D. virilis and their hybrids. Anti-Vasa staining indicated that the major loss of pole cells occurs in dysgenic embryos at stage 11-14 after primordial germ cells (PGC) pass the midgut wall. At later ontogenetic stages, including larvae, pupae and imagoes, we often observed an abnormal development of gonads in dysgenic individuals with a frequent occurrence of unilateral and bilateral gonadal atrophy. Dysgenic females were characterized by the presence of various sterile ovarian phenotypes that predominantly include agametic ovarioles, while other atypical forms such as tumor-like ovarioles and dorsalized ovariolar follicles may also be present. Testis abnormalities were also frequently observed in dysgenic males. The sterility manifestations depended on the strain, the growing temperature and the age of the flies used in crosses. The observed gonadal sterility and other HD manifestations correlated with the absence of maternal piRNAs homologous to Penelope and other transposons in the early dysgenic embryos. We speculate that gonadal abnormalities mimicking several known sterility mutations probably result from the disturbance of developmental gene expression machinery due to the activation of unrelated families of transposons in early dysgenic embryos.