THE RECA GENE OF STREPTOCOCCUS-PNEUMONIAE IS PART OF A COMPETENCE-INDUCED OPERON AND CONTROLS LYSOGENIC INDUCTION

THE RECA GENE OF STREPTOCOCCUS-PNEUMONIAE IS PART OF A COMPETENCE-INDUCED OPERON AND CONTROLS LYSOGENIC INDUCTION
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DOI:
10.1111/j.1365-2958.1995.tb02250.x
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发表时间:
1995-01-01
影响因子:
3.6
通讯作者:
CLAVERYS, JP
CLAVERYS, JP
中科院分区:
生物学2区
文献类型:
--
作者:
MARTIN, B;GARCIA, P;CLAVERYS, JP

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最近发现的recA基因的自然转化细菌肺炎链球菌已进一步通过构建recA无效突变和研究其调节。recA突变已被证明赋予DNA修复(根据对紫外线和甲基甲烷磺酸盐的敏感性判断)和重组缺陷。质粒转化为recA突变体也急剧减少。蛋白质印迹法确定,recA基因表达增加了几倍,在发病的能力,遗传转化。增加的表达与recA特异性转录物的出现有关,约5.7 kb长。该转录本表明recA是感受态诱导(cin)操纵子的一部分。从非感受态细胞中检测到的主要(约4.3 kb)转录物不包括操纵子中的第一个基因cinA,这表明该基因可能在转化过程的某些阶段是特异性需要的。在用丝裂霉素C处理的细胞中检测到少量的5.7 kb多顺反子mRNA,表明操纵子也可以是损伤诱导的。此外,丝裂霉素C处理recA(-)溶原性菌株不会导致原噬菌体诱导和细胞裂解。这与recA(+)溶原菌的情况不同。这些结果共同表明RecA控制溶原诱导,并表明在S.肺炎。
The recently identified recA gene of the naturally transformable bacterium Streptococcus pneumoniae has been further characterized by constructing a recA null mutation and by investigating its regulation. The recA mutation has been shown to confer both DNA repair (as judged from sensitivity to u.v. and methyl methane sulphonate) and recombination deficiencies, Plasmid transformation into the recA mutant was also drastically reduced. Western blotting established that recA gene expression is increased several fold at the onset of competence for genetic transformation. Increased expression was associated with the appearance of a recA-specific transcript, approximately 5.7 kb long. This transcript indicated that recA is part of a competence-inducible (cin) operon. The major (about 4.3 kb) transcript detected from non-competent cells did not include cinA, the first gene in the operon, suggesting that this gene could be specifically required at some stage in the transformation process. Detection of small amounts of the 5.7 kb polycistronic mRNA in cells treated with mitomycin C suggested that the operon could also be damage inducible. In addition, mitomycin C treatment of a recA(-) lysogenic strain did not lead to prophage induction and cell lysis. This is unlike the situation of a recA(+) lysogen. Together these results demonstrate that RecA controls lysogenic induction and suggest the existence of a SOS repair system in S. pneumoniae.