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LexA cleavage is required for CTX prophage induction

机译:LexA裂解是CTX预噬诱导所必需的

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摘要

The physiologic conditions and molecular interactions that control phage production have been studied in few temperate phages. We investigated the mechanisms that regulate production of CTXphi, a temperate filamentous phage that infects Vibrio cholerae and encodes cholera toxin. In CTXphi lysogens, the activity of P-rstA the only CTXphi P promoter required for CTX prophage development, is repressed by RstR, the CTXphi repressor. We found that the V. cholerae SOS response regulates CTXphi production. The molecular mechanism by which this cellular response to DNA damage controls CTXphi production differs from that by which the E coli SOS response controls induction of many prophages. UV-stimulated CTXphi production required RecA-dependent autocleavage of LexA, a repressor that controls expression of numerous host DNA repair genes. LexA and RstR both bind to and repress P-rstA.Thus, CTXphi production is controlled by a cellular repressor whose activity is regulated by the cell's response to DNA damage.
机译:已经在少数温带噬菌体中研究了控制噬菌体产生的生理条件和分子相互作用。我们研究了调节CTXphi产生的机制,CTXphi是一种温和的丝状噬菌体,可感染霍乱弧菌并编码霍乱毒素。在CTXphi溶原菌中,CTX噬菌体发育所需的唯一CTXphi P启动子P-rstA的活性被CTXphi阻遏物RstR抑制。我们发现霍乱弧菌的SOS反应调节了CTXphi的产生。这种细胞对DNA损伤的反应控制CTXphi产生的分子机制不同于大肠杆菌SOS反应控制许多噬菌体的诱导的分子机制。紫外线刺激的CTXphi生产需要LexA依赖RecA的自动切割,LexA是控制许多宿主DNA修复基因表达的阻遏物。 LexA和RstR都与P-rstA结合并抑制P-rstA,因此CTXphi的产生受细胞阻遏物控制,其活性受细胞对DNA损伤的反应所调节。

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