Allgood N D, Silhavy T J
Department of Molecular Biology, Princeton University, New Jersey 08544-1014.
Genetics. 1991 Apr;127(4):671-80. doi: 10.1093/genetics/127.4.671.
Mutations of Escherichia coli K-12 were isolated that increase the frequency of deletion formation. Three of these mutations map to the gene sbcB at 43.5 min on the E. coli chromosome. Two types of mutations at sbcB have been previously defined: sbcB-type that suppress both the UV sensitivity and recombination deficiency of recBC mutants, and xonA-type that suppress only the UV sensitivity. Both types are defective for production of exonuclease I activity. The mutations isolated here were similar to xonA alleles of sbcB because they suppressed the UV sensitivity of recBC mutants but did not restore recombination proficiency. Indeed, two previously characterized xonA alleles were shown to increase the frequency of deletion formation, although an sbcB allele did not. This result demonstrates that loss of exonuclease I activity is not sufficient to confer a high deletion phenotype, rather, the product of the sbcB gene possesses some other function that is important for deletion formation. Because deletion formation in this system is recA independent and does not require extensive DNA homology, these mutations affect a pathway of illegitimate recombination.
分离出了增加缺失形成频率的大肠杆菌K - 12突变体。其中三个突变定位于大肠杆菌染色体上43.5分钟处的sbcB基因。先前已定义了sbcB的两种突变类型：sbcB型，可抑制recBC突变体的紫外线敏感性和重组缺陷；xonA型，仅抑制紫外线敏感性。两种类型在外切核酸酶I活性产生方面均有缺陷。此处分离出的突变体与sbcB的xonA等位基因相似，因为它们抑制了recBC突变体的紫外线敏感性，但未恢复重组能力。实际上，两个先前已鉴定的xonA等位基因显示可增加缺失形成频率，而一个sbcB等位基因则不然。这一结果表明，外切核酸酶I活性的丧失不足以赋予高缺失表型，相反，sbcB基因的产物具有一些对缺失形成很重要的其他功能。由于该系统中的缺失形成不依赖recA且不需要广泛的DNA同源性，这些突变影响了异常重组途径。
