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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Studies on mutagen-sensitive strains of Drosophila melanogaster. VI. The effect of DNA-repair deficiencies in spermatids, spermatocytes and spermatogonia irradiated in N2 or O2.

This study was aimed at ascertaining the extent to which paternal repair processes possibly deficient in mei-9a, mei-41D5 and mus-101D1 genotypes would affect the recovery of radiation-induced recessive lethals in early spermatids, spermatocytes and spermatogonia. These germ cell stages were sampled in two 2-day broods from freshly hatched males, that were irradiated as 24-h old pupae in O2, or N2 followed by N2 or O2 post-treatment. Spontaneous mutation frequencies were higher in mei-9 and mei-41 males, and thus appropriate corrections were applied to the radiation data. Only with mei-9 males a clear and consistent increase of the radiation-induced mutation frequency was observed. The effect is somewhat more pronounced in brood B, presumably representing spermatogonia, than in brood A and is observed after radiation in either O2 or N2. The paternal repair process thus differs from the maternal one in that it also responds to radiation damage induced in O2. The finding that, following irradiation under anoxia, post-treatment with O2 (versus that with N2), also lowers the mutation frequency in mei-9 males, indicates that the repair defect in mei-9 does not interfere with oxygen-dependent post-radiation repair. Thus there are two different paternal repair processes in these early stages of spermatogenesis: that is, one controlled by mei-9 and one depending on oxygen. Mei-41 and mus-101 do not appear to interfere with the paternal repair process. The frequency of translocations recovered from these stages was likewise not affected by mus-101.[1]


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