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Involvement of inorganic polyphosphate in expression of SOS genes

机译:无机多磷酸盐参与SOS基因的表达

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Inorganic polyphosphate (poly(P)) is a linear polymer that has been found in every organism so far examined. To elucidate the functions of poly(P) in the regulation of gene expression, the level of cellular poly(P) in Escherichia coli was reduced to a barely detectable concentration by overproduction of exopolyphosphatase (exopoly(P)ase) with a plasmid encoding yeast exopoly(P)ase (Shiba et al., Proc. Natl. Acad. Sci. USA 94 (1997) 11210-11215). It was found that exopoly(P)ase-overproducing cells were more sensitive to UV or mitomycin C (MMC) than were control cells. Poly(P) accumulation was observed after treatment with MMC, whereas the poly(P) level was below the detectable level in cells that overproduced exopoly(P)ase. When exopoly(P)ase-overproducing cells were transformed again by a multiple copy number plasmid that carries the polyphosphate kinase gene (ppk), the cells accumulated a great amount of poly(P) and restored the UV and MMC sensitivities to the level of control cells. In exopoly(P)ase-overproducing cells, the expression of recA and umuDC were not induced by MMC. In addition, a strain containing multiple copies of ppk accumulated not only a large amount of poly(P) but also recA mRNA. Since recA expression was induced in a recA-deletion strain harboring a plasmid with the ppk gene, poly(P) could be necessary for regulating the expression of SOS genes without depending on the RecA-LexA regulatory network.
机译:无机多磷酸盐(poly(P))是一种线性聚合物,迄今为止已在每种生物中发现。为了阐明poly(P)在基因表达调控中的功能,通过用编码酵母的质粒过量生产exopolyphosphatase(exopoly(P)ase),将大肠杆菌中细胞poly(P)的水平降至几乎检测不到的浓度。 exopoly(P)酶(Shiba等人,Proc.Natl.Acad.Sci.USA 94(1997)11210-11215)。发现外泌(P)酶过量细胞比对照细胞对UV或丝裂霉素C(MMC)更敏感。用MMC处理后观察到Poly(P)积累,而在过量产生exopoly(P)酶的细胞中,poly(P)水平低于可检测水平。当携带多聚磷酸激酶基因(ppk)的多拷贝数质粒再次转化产生外聚(P)酶的细胞时,细胞会积累大量的聚(P),并将UV和MMC敏感性恢复到控制细胞。在exopoly(P)ase过量生产细胞中,MMC不会诱导recA和umuDC的表达。另外,含有多个ppk拷贝的菌株不仅积累了大量的poly(P),而且还积累了recA mRNA。由于recA表达是在带有ppk基因质粒的recA缺失菌株中诱导的,因此poly(P)对于调节SOS基因的表达可能是必需的,而不依赖于RecA-LexA调控网络。

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