Relationships among chromatid interchanges, sister chromatid exchanges, and meiotic recombination in Drosophila melanogaster

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Abstract
Repair- and recombination-defective mutations at 2 loci (mei-9 and mei-41) of D. melanogaster were examined for their effects on the induction of chromosome aberrations by X-rays and the formation of sister chromatid exchanges (SCE). Irradiation of larval neuroblast cells during the S phase with X-rays showed that mutants at both of these loci are about 10 times more sensitive than wild type to the induction of chromosome aberrations. The pattern of induced aberrations was characteristic for each mutant locus: in cells bearing mei-9 mutations most breaks were chromatid deletions, whereas in the presence of mei-41 mutations similar frequencies of chromatid and isochromatid deletions were observed. Chromatid interchanges could not be induced in cells carrying mei-9 alleles; therefore these mutations define a step necessary for chromatid rejoining. The mei-41 alleles also define a function involved in the formation of chromatid interchanges; total exchanges were less frequent than expected from nonmutant controls; and the proportion of exchanges arising by symmetrical rejoining was markedly reduced. Chromatid and isochromatid deletions have different molecular steps in their formation, and different molecular mechanisms are also involved in the symmetrical and unsymmetrical rejoining in chromatid interchanges. Neuroblast cells of larvae bearing mei-9 and mei-41 alleles were also treated for 13 h with 5-bromodeoxyuridine at 9 .mu.g/ml to differentiate sister chromatids for the scoring of SCE. Whereas mei-41 had a normal level of SCE, mei-9 exhibited a frequency of SCE that was about 70% that of the control. Because both mei-9 and mei-41 mutations result in defective meiotic recombination, they may define steps shared by symmetrical interchange formation and meiotic recombination that do not participate in the formation of most SCE.