DNA double-strand break repair: genetic determinants of flanking crossing-over.
Whether or not homologous interaction of two DNA molecules results in crossing-over of the flanking sequences is an important decision in view of genome organization. Several homologous recombination models, including the double-strand break repair models, explain this decision as choice between two alternative modes of resolution of Holliday-type intermediates. We have demonstrated that a double-strand gap can be repaired through gene conversion copying a homologous duplex, as predicted by the double-strand break repair models, in the RecE pathway of Escherichia coli. This gap repair is often accompanied by crossing-over of the flanking sequences. Mutations in ruvC and recG, whose products interact with Holliday structures in vitro, do not block double-strand gap repair or its association with flanking crossing-over. However, two mutations in the recJ gene, which encodes a single-strand 5'-->3' exonuclease, severely decrease association of flanking crossing-over. Two mutations in the recQ gene, which encodes a helicase, moderately decrease association of flanking crossing-over by themselves and suppress the severe effect of a recJ mutation. Similar relationships of recJ and recQ mutations are observed in cell survival after ultraviolet light irradiation, gamma-ray irradiation, and H2O2 treatment. We discuss how cooperation of the recQ gene product and the recJ gene product brings about double-strand break repair accompanied by flanking crossing-over. We also discuss how this reaction is related to repair of chromosome damages.
Kusano
K
K
Department of Molecular Biology, University of Tokyo, Japan.
Sunohara
Y
Y
Takahashi
N
N
Yoshikura
H
H
Kobayashi
I
I
D000251:Adenosine Triphosphatases / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D003434:Crossing Over, Genetic; D004249:DNA Damage; D004265:DNA Helicases / Q000235:genetics; D004260:DNA Repair / Q000235:genetics*; D004269:DNA, Bacterial / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D004706:Endodeoxyribonucleases; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D029968:Escherichia coli Proteins; D005090:Exodeoxyribonucleases; D005720:Gamma Rays; D005785:Gene Conversion; D005798:Genes, Bacterial; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008957:Models, Genetic; D009154:Mutation; D053484:RecQ Helicases; D011995:Recombination, Genetic; D014170:Transformation, Genetic; D014466:Ultraviolet Rays
D001426:Bacterial Proteins; D004269:DNA, Bacterial; D029968:Escherichia coli Proteins; C069806:ruvC protein, E coli; C071446:RecG protein, E coli; D006861:Hydrogen Peroxide; D004706:Endodeoxyribonucleases; D005090:Exodeoxyribonucleases; C489467:RecJ protein, E coli; C070765:recJ protein, Bacteria; D000251:Adenosine Triphosphatases; C506724:RecQ protein, E coli; D004265:DNA Helicases; D053484:RecQ Helicases