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大肠杆菌中与SOS反应相关的细胞分裂抑制新机制。

Novel mechanism of cell division inhibition associated with the SOS response in Escherichia coli.

作者信息

D'Ari R, Huisman O

出版信息

J Bacteriol. 1983 Oct;156(1):243-50. doi: 10.1128/jb.156.1.243-250.1983.

Abstract

Certain Escherichia coli strains were shown to possess a novel system of cell division inhibition, called the SfiC+ phenotype. SfiC+ filamentation had a number of properties similar to those of sfiA-dependent division inhibition previously described: (i) both are associated with the SOS response induced by expression of the recA(Tif) mutation, (ii) both are associated with cell death, (iii) both are amplified in mutants lacking the Lon protease, and (iv) both are suppressed by sfiB mutations. SfiC+ filamentation and sfiA-dependent division inhibition differed in (i) the physiological conditions under which loss of viability is observed, (ii) the extent of amplification in lon mutants, (iii) their genetic regulation (SfiC+ filamentation is not under direct negative control of the LexA repressor), and (iv) their genetic determinants (SfiC+ filamentation depends on a locus, sfiC+, near 28 min on the E. coli map and distinct from sfiA).

摘要

某些大肠杆菌菌株被证明拥有一种新型的细胞分裂抑制系统,称为SfiC + 表型。SfiC + 丝状化具有许多与先前描述的依赖sfiA的分裂抑制相似的特性:(i)两者都与recA(Tif)突变表达诱导的SOS反应相关,(ii)两者都与细胞死亡相关,(iii)两者在缺乏Lon蛋白酶的突变体中都会增强,并且(iv)两者都被sfiB突变抑制。SfiC + 丝状化和依赖sfiA的分裂抑制在以下方面有所不同:(i)观察到活力丧失的生理条件,(ii)lon突变体中的增强程度,(iii)它们的基因调控(SfiC + 丝状化不受LexA阻遏物的直接负调控),以及(iv)它们的遗传决定因素(SfiC + 丝状化取决于大肠杆菌图谱上28分钟附近的一个位点sfiC + ,且与sfiA不同)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e3/215076/6004ff45e580/jbacter00239-0255-a.jpg

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