Abstract
Gonadal atrophy is the most typical and dramatic manifestation of intraspecific hybrid dysgenesis syndrome leading to sterility in Drosophila melanogaster dysgenic progeny. The P-M system of hybrid dysgenesis is primarily associated with germ cell degeneration during the early stages of Drosophila embryonic development at elevated temperatures. In the present study, we have defined the phase of germ cell death as beginning at the end of embryogenesis immediately following gonad formation. However, the temperature-dependent screening of germ cell developmental patterns in the dysgenic background showed that early germ cells are susceptible to the hybrid dysgenesis at any Drosophila life-cycle stage, including in the imago. Electron microscopy of germ cells after dysgenesis induction revealed significant changes in subcellular structure, especially mitochondria, prior to cellular breakdown. The mitochondrial pathology can promote the activation of cell death pathways in dysgenic germ cells, which leads to gonadal atrophy.
Highlights
Crosses between some pairs of Drosophila melanogaster strains result in the sterility of hybrid offspring in one cross direction, which is most clearly manifested in females
Dysgenesis (PM HD) (Sved, 1976; Kidwell et al, 1977). Such PM gonadal dysgenesis (GD) is susceptible to developmental temperature and is strongly displayed when dysgenic flies are raised at restrictive temperatures of 25– 29 °C
We propose that cell death pathways are activated by mitochondrial dysfunction, and that the mitochondrial defects may result from nuclearcytoplasmic conflict in the P-M system of HD
Summary
Crosses between some pairs of Drosophila melanogaster strains result in the sterility of hybrid offspring in one cross direction, which is most clearly manifested in females. It is believed that such events are the result of interaction of the paternal (P) genome with the maternal (M) cytoplasm. Dysgenic gonads contain an extremely reduced number of germ cells (GCs), a normal somatic background is maintained (Kidwell and Novy, 1979; Engels and Preston, 1979; Bhat and Schedl, 1997). To understand why the germ cells do not survive in the dysgenic background we monitored their development cytologically during the fly life cycle under various temperature conditions. We propose that cell death pathways are activated by mitochondrial dysfunction, and that the mitochondrial defects may result from nuclearcytoplasmic conflict in the P-M system of HD
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