SOS induction in a subpopulation of structural maintenance of chromosome (Smc) mutant cells in Bacillus subtilis
SOS induction in a subpopulation of structural maintenance of chromosome (Smc) mutant cells in Bacillus subtilis
复制标题
DOI：
10.1128/jb.00132-07
复制
发表时间：
2007-06-01
影响因子：
3.2
通讯作者：
Grossman, Alan D.
中科院分区：
文献类型：
--
作者：
Britton, Robert A.;Kuster-Schock, Elke;Grossman, Alan D.
染色体结构维持蛋白（Smc）是一种高度保守的蛋白质，参与染色体的紧密结合和其他DNA相关过程。在枯草芽孢杆菌中，smc无效突变导致DNA超螺旋、染色体压实和染色体分配缺陷。我们研究了正弦突变对B中整体基因表达的影响。枯草芽孢杆菌的DNA微阵列。我们发现，smc无效突变引起SOS反应的部分诱导，包括诱导有缺陷的原噬菌体PBSX。SOS和噬菌体基因在单细胞中表达的分析表明，大约1%的smc突变体完全诱导SOS和PBSX基因表达，而其他99%的细胞似乎有很少或没有表达。我们发现，PBSX的诱导不是smc突变体的染色体分配或压缩缺陷的原因。类似的诱导SOS反应和PBSX中观察到的拓扑异构酶I，负超螺旋DNA松弛酶耗尽的细胞。
The structural maintenance of chromosome (Smc) protein is highly conserved and involved in chromosome compaction, cohesion, and other DNA-related processes. In Bacillus subtilis, smc null mutations cause defects in DNA supercoiling, chromosome compaction, and chromosome partitioning. We investigated the effects of sine mutations on global gene expression in B. subtilis using DNA microarrays. We found that an smc null mutation caused partial induction of the SOS response, including induction of the defective prophage PBSX. Analysis of SOS and phage gene expression in single cells indicated that approximately 1% of smc mutants have fully induced SOS and PBSX gene expression while the other 99% of cells appear to have little or no expression. We found that induction of PBSX was not responsible for the chromosome partitioning or compaction defects of smc mutants. Similar inductions of the SOS response and PBSX were observed in cells depleted of topoisomerase I, an enzyme that relaxes negatively supercoilled DNA.