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Homologous Recombination and DNA Double-strand Breaks

同源重组和 DNA 双链断裂

基本信息

批准号：
01580251
负责人：
KOBAYASHI Ichizo
金额：
$ 1.66万
依托单位：
University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-01580251/
关键词：
Genetic recombination Homologous recombination DNA repair recA E. coli Tumor virus BPV BPV がんウイルス遺伝子変換ラムダプラスミド遺伝子

项目摘要

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.

1.λ基因重组的双链断裂修复模型。(1)证明了双链缺口修复。(2)Redalpha和redbeta只是这种修复所必需的lambda基因。(3)RecA、recBC、recD、recJ、recN和ruvB基因的功能。大肠杆菌不是必需的。(4)RecA蛋白可能影响交叉与非交叉的选择。我们建立了一个质粒转移系统，可以回收两种重组产物，并显示：（1）E.大肠杆菌是不可逆的。(2)双链断裂刺激重组，夸大了这种非互惠的性质。(3)这些结果支持“连续半交换模型”，即一个重组事件产生一个DNA末端，然后刺激下一个重组事件.在大肠杆菌的RecE途径中，我们证明了以下几点：（1）双链断裂刺激相互的双链缺口修复。(2)双链末端的修饰使得重组是非相互的，但不改变其频率。(3)这些结果使我们建立了一个模型，在该模型中，双链缺口的产生导致以下三种途径之一：非相互重组、有交换的相互双链缺口修复和没有交换的相互双链缺口修复。我们分析了哺乳动物同源重组，特别是BPV质粒的基因打靶。