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Title: DNA double-strand break repair: Genetic determinants of flanking crossing-over

Journal Article · · Proceedings of the National Academy of Sciences of the United States of America; (United States)

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. The authors 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[prime][yields]3[prime] 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 H[sub 2]O[sub 2] treatment. The authors discuss how cooperation of the recQ gene product and the recJ gene product brings about double-strand break repair accompanied by flanking crossing-over. They also discuss how this reaction is related to repair of chromosome damages.

OSTI ID:
7009335
Journal Information:
Proceedings of the National Academy of Sciences of the United States of America; (United States), Vol. 91:3; ISSN 0027-8424
Country of Publication:
United States
Language:
English