1990 Fiscal Year Final Research Report Summary
Homologous Recombination and DNA Double-strand Breaks
| Project/Area Number |
01580251
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
分子遺伝学・分子生理学
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| Research Institution | University of Tokyo |
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Principal Investigator |
KOBAYASHI Ichizo Institute of Medical Science, University of Tokyo, Associate Professor, 医科学研究所, 助教授 (30126057)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Genetic recombination / Homologous recombination / Homologous recombination / DNA repair / recA / E. coli / Tumor virus / BPV |
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| Research Abstract |
1. On double-strand break repair model for recombination by lambda. (1) Proved double-strand gap repair. (2) Redalpha and redbeta are only lambda genes essential to this repair. (3) RecA, recBC, recD, recJ, recN, and ruvB gene functions of E. coli are not essential. (4) RecA protein might affect choice between crossover and non-crossover.
2. We made a plasmid transfer system that allows recovery of both products of recombination and showed:(1) RecF pathway of E. coli is non-reciprocal. (2) A double-strand break stimulates recombination exaggerating this non-reciprocal nature. (3) These results support "successive half crossing-over model", which proposes that one event of recombination makes a DNA end that then stimulates a next event of recombination.
3. We demonstrated the following in RecE pathway of E. coli: (1) A double strand break stimulates reciprocal double-strand gap repair. (2) Modification of a double strand end makes recombination non-reciprocal but does not alter its frequency. (3) These results led us to a model in which creation of a double-strand gap leads to one of the following three pathways: non-reciprocal recombination, reciprocal double-strand gap repair with crossing-over, and reciprocal double-strand gap repair without crossing-over.
4. We analyzed mammalian homologous recombination especially gene targeting with BPV plasmid.
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