A high level of hybrid dysgenesis in Drosophila: high thermosensitivity, dependence on DNA repair, and incomplete cytotype regulation.
An unusually high level of P-M hybrid dysgenesis in Drosophila melanogaster is characteristic of hybrid offspring originating from both, A (M female x P male) and B (P female x M male) crosses of a subline of the Harwich P strain, termed Hs. The novel properties induced by mobility of P elements carried by Hs paternal chromosomes include: very high (over 95%) gonadal dysgenesis (GD) in both sexes at the low restrictive temperature of 21 degrees C, and highly premature sterility when males are reared at 18 degrees C and aged at 21 degrees C. Although all three major chromosomes of the Hs subline contributed to this atypical pattern of gonadal dysgenesis, chromosome 3 had the largest effect. Gonadal dysgenesis showed a temperature- and sex-dependent repression pattern by the defective P elements of Muller-5 Birmingham chromosomes; at 21 degrees C there was virtually no repression of male sterility, but most effective repression of GD in females. At 29 degrees C repression was effective in males, but declined in females. The high thermosensitive sterility, low fecundity, and premature aging of the male germ line were greatly exacerbated when males derived from either A or B crosses were deficient either in excision repair (mei-9 mutation) or in post-replication repair (mei-41 mutation). These findings demonstrate that both DNA repair pathways are essential for the repair of lesions induced by P element transposition and support the hypothesis that P element-induced chromosome breaks are responsible for the virtual abolition of the germ line. The relatively high premature sterility of cross B DNA repair-deficient males, reared at 18 degrees C and aged at 21 degrees C, indicates that there is incomplete cytotype regulation in Hs subline hybrids.[1]References
- A high level of hybrid dysgenesis in Drosophila: high thermosensitivity, dependence on DNA repair, and incomplete cytotype regulation. Margulies, L. Mol. Gen. Genet. (1990) [Pubmed]
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