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位点特异性甲基化酶在大肠杆菌中诱导SOS DNA修复反应。

Site-specific methylases induce the SOS DNA repair response in Escherichia coli.

作者信息

Heitman J, Model P

出版信息

J Bacteriol. 1987 Jul;169(7):3243-50. doi: 10.1128/jb.169.7.3243-3250.1987.

Abstract

Expression of the site-specific adenine methylase HhaII (GmeANTC, where me is methyl) or PstI (CTGCmeAG) induced the SOS DNA repair response in Escherichia coli. In contrast, expression of methylases indigenous to E. coli either did not induce SOS (EcoRI [GAmeATTC] or induced SOS to a lesser extent (dam [GmeATC]). Recognition of adenine-methylated DNA required the product of a previously undescribed gene, which we named mrr (methylated adenine recognition and restriction). We suggest that mrr encodes an endonuclease that cleaves DNA containing N6-methyladenine and that DNA double-strand breaks induce the SOS response. Cytosine methylases foreign to E. coli (MspI [meCCGG], HaeIII [GGmeCC], BamHI [GGATmeCC], HhaI [GmeCGC], BsuRI [GGmeCC], and M.Spr) also induced SOS, whereas one indigenous to E. coli (EcoRII [CmeCA/TGG]) did not. SOS induction by cytosine methylation required the rglB locus, which encodes an endonuclease that cleaves DNA containing 5-hydroxymethyl- or 5-methylcytosine (E. A. Raleigh and G. Wilson, Proc. Natl. Acad. Sci. USA 83:9070-9074, 1986).

摘要

位点特异性腺嘌呤甲基化酶HhaII(GmeANTC,其中me表示甲基化)或PstI(CTGCmeAG)的表达在大肠杆菌中诱导了SOS DNA修复反应。相比之下,大肠杆菌自身的甲基化酶表达要么不诱导SOS反应(EcoRI [GAmeATTC]),要么诱导SOS反应的程度较小(dam [GmeATC])。对腺嘌呤甲基化DNA的识别需要一个先前未描述基因的产物,我们将其命名为mrr(甲基化腺嘌呤识别与限制)。我们认为mrr编码一种核酸内切酶,该酶可切割含有N6 - 甲基腺嘌呤的DNA,并且DNA双链断裂会诱导SOS反应。大肠杆菌外源性的胞嘧啶甲基化酶(MspI [meCCGG]、HaeIII [GGmeCC]、BamHI [GGATmeCC]、HhaI [GmeCGC]、BsuRI [GGmeCC]和M.Spr)也诱导了SOS反应,而大肠杆菌自身的一种(EcoRII [CmeCA/TGG])则没有。胞嘧啶甲基化诱导SOS反应需要rglB基因座,该基因座编码一种核酸内切酶,可切割含有5 - 羟甲基胞嘧啶或5 - 甲基胞嘧啶的DNA(E.A.罗利和G.威尔逊,《美国国家科学院院刊》83:9070 - 9074,1986年)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4533/212376/0e0436eb3163/jbacter00197-0346-a.jpg

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