Ball T K, Wasmuth C R, Braunagel S C, Benedik M J
Department of Biology, Texas A&M University, College Station 77843-3258.
J Bacteriol. 1990 Jan;172(1):342-9. doi: 10.1128/jb.172.1.342-349.1990.
A previously described regulatory mutation which abolishes expression of the extracellular nuclease of Serratia marcescens is shown to be a mutation of the Serratia recA gene. The defect in nuclease expression could be restored by introducing a plasmid carrying the recA gene of Escherichia coli. The DNA sequence of the Serratia gene is very similar to that of the E. coli gene. The putative LexA-binding site of the Serratia recA gene is almost identical to that of E. coli, along with the promoter. A similar LexA-binding site can also be found upstream of the nuclease gene. As expected from this finding, we show that nuclease expression can be induced by SOS-inducing agents such as mitomycin C. Although inducible in S. marcescens, the nuclease was expressed only at the uninduced levels in E. coli and could not be induced by mitomycin C. The extracellular chitinase and lipase were similarly affected by the mutations altering nuclease expression and were also induced by mitomycin C.
一种先前描述的能消除粘质沙雷氏菌胞外核酸酶表达的调控突变,被证明是沙雷氏菌recA基因的突变。通过引入携带大肠杆菌recA基因的质粒,核酸酶表达缺陷得以恢复。沙雷氏菌基因的DNA序列与大肠杆菌基因非常相似。沙雷氏菌recA基因的假定LexA结合位点与大肠杆菌的几乎相同,启动子也是如此。在核酸酶基因上游也能发现类似的LexA结合位点。基于这一发现,正如预期的那样,我们表明核酸酶表达可被丝裂霉素C等SOS诱导剂诱导。虽然在粘质沙雷氏菌中可诱导,但核酸酶在大肠杆菌中仅以未诱导水平表达,且不能被丝裂霉素C诱导。胞外几丁质酶和脂肪酶同样受到改变核酸酶表达的突变的影响,并且也能被丝裂霉素C诱导。