Open AccessRelationships among chromatid interchanges, sister chromatid exchanges, and meiotic recombination in Drosophila melanogaster
Author(s) -
Maurizio Gatti,
Sergio Pimpinelli,
Bruce S. Baker
Publication year - 1980
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.77.3.1575
Subject(s) - chromatid , sister chromatids , genetics , biology , drosophila melanogaster , microbiology and biotechnology , allele , chromosome , gene
Repair- and recombination-defective mutations at two loci (mei-9 andmei-41 ) ofDrosophila melanogaster have been examined for their effects on the induction of chromosome aberrations by x-rays and the formation of sister chromatid exchanges (SCEs). 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 bearingmei-9 mutations most breaks were chromatid deletions, whereas in the presence ofmei-41 mutations similar frequencies of chromatid and isochromatid deletions were observed. Furthermore, chromatid interchanges could not be induced in cells carryingmei-9 alleles; therefore these mutations define a step necessary for chromatid rejoining.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. These data indicate that chromatid and isochromatid deletions have different molecular steps in their formation, and that different molecular mechanisms are also involved in the symmetrical and unsymmetrical rejoining in chromatid interchanges. Neuroblast cells of larvae bearingmei-9 andmei-41 alleles were also treated for 13 hr with 5-bromodeoxyuridine at 9 μg/ml in order to differentiate sister chromatids for the scoring of SCEs. Whereasmei-41 had a normal level of SCEs,mei-9 exhibited a frequency of SCEs that was about 70% that of the control. Because bothmei-9 andmei-41 mutations result in defective meiotic recombination, these data suggest that they define steps shared by symmetrical interchange formation and meiotic recombination that do not participate in the formation of most SCEs.