Ontogenetic consequences of dysgenic crosses in Drosophila virilis

Abstract

Hybrid 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.

Hybrid dysgenesis in Drosophila virilis results in clusters of mitotic recombination and loss-of-heterozygosity but leaves meiotic recombination unaltered

“…GSCs marked with the mitotic CO were thus able to recover and rescue fertility after hybrid dysgenesis in the high fecundity female. This is consistent with the observation that hybrid dysgenesis is associated with an early phase of germline depletion [29].…”

“…Similar to other systems, dysgenesis occurs when females lacking a given TE family are mated with males that carry them. Developmentally, it is more similar to the P-M rather than I-R system of dysgenesis in D. melanogaster because the events that cause sterility happen in the early germline [28,29]. However, in contrast to the P-M system, sterility appears to be due to the mass activation of multiple TE families abundant in strain 160 but not strain 9.…”

Whole genome sequencing in Drosophila virilis identifies Polyphemus, a recently activated Tc1-like transposon with a possible role in hybrid dysgenesis

“…In light of this, it is important to note that the sterility syndrome is evident early in development [33], not at the time that gonadal expression is typically measured. For this reason, TE expression in adult females that have escaped sterility - a necessary condition for measuring germline gene expression - may not be a perfect proxy for understanding TE expression early in development.…”

Spontaneous gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis

“…Despite significant progress in understanding the morphogenetic events occurring during gametogenesis and embryogenesis in the progeny of D . virilis dysgenic crosses, these questions still need to be answered [ 11 , 18 ].…”