Genome rearrangement in top3 mutants of Saccharomyces cerevisiae requires a functional RAD1 excision repair gene.
Genome rearrangement in top3 mutants of Saccharomyces cerevisiae requires a functional RAD1 excision repair gene.
复制标题
酿酒酵母 top3 突变体中的基因组重排需要功能性 RAD1 切除修复基因。
DOI：
10.1128/mcb.12.11.4988-4993.1992
复制
发表时间：
1992
影响因子：
5.3
通讯作者：
Rothstein,R
中科院分区：
文献类型：
--
作者：
Bailis,AM;Arthur,L;Rothstein,R
酿酒酵母TOP3是一种编码与细菌I型拓扑异构酶同源的蛋白质的基因，突变的酿酒酵母细胞具有多种缺陷，包括生长速度减慢，基因表达改变，产孢量受阻，几个基因位点的有丝分裂重组率上升。在含有atop3零突变的细胞中，两个互不相连的同源基因座SAM1和SAM2之间的异位重组率是野生型细胞的6倍。另外两个已知的拓扑异构酶基因INS中的任何一个发生突变。酿酒酵母TOP1和TOP2不影响SAM基因之间的重组率。Op3突变还改变了SAM基因之间重组事件的分布，导致了新的缺失-插入事件的出现，其中转换区延伸到编码序列之外，用另一个基因3‘端两侧的非同源DNA取代了一个SAM基因3’端两侧的DNA。Top3缺失突变对重组的影响依赖于完整的RADI切除修复基因的存在，因为与Top3突变相比，Top3突变细胞的异位基因转化率和转化通道长度都降低了。这些结果表明，依赖于aRAD1的功能参与了由于top3活性丧失而导致的DNA损伤的处理，目的是通过重组修复这些DNA。
Saccharomyces cerevisiaecells that are mutated atTOP3, a gene that encodes a protein homologous to bacterial type I topoisomerases, have a variety of defects, including reduced growth rate, altered gene expression, blocked sporulation, and elevated rates of mitotic recombination at several loci. The rate of ectopic recombination between two unlinked, homeologous loci,SAM1andSAM2, is sixfold higher in cells containing atop3null mutation than in wild-type cells. Mutations in either of the two other known topoisomerase genes inS. cerevisiae, TOP1andTOP2, do not affect the rate of recombination between theSAMgenes. Thetop3mutation also changes the distribution of recombination events between theSAMgenes, leading to the appearance of novel deletion-insertion events in which conversion tracts extend beyond the coding sequence, replacing the DNA flanking the3'end of oneSAMgene with nonhomologous DNA flanking the3fend of the other. The effects of thetop3null mutation on recombination are dependent on the presence of an intactRADIexcision repair gene, because both the rate ofSAMectopic gene conversion and the conversion tract length were reduced inradl top3mutant cells compared withtop3mutants. These results suggest that aRAD1-dependent function is involved in the processing of damaged DNA that results from the loss of Top3 activity, targeting such DNA for repair by recombination.