REVERSIBILITY OF SOS-ASSOCIATED DIVISION INHIBITION IN ESCHERICHIA-COLI
REVERSIBILITY OF SOS-ASSOCIATED DIVISION INHIBITION IN ESCHERICHIA-COLI
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DOI：
10.1128/jb.166.3.733-738.1986
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发表时间：
1986-06-01
影响因子：
3.2
通讯作者：
DARI, R
中科院分区：
文献类型：
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作者：
MAGUIN, E;LUTKENHAUS, J;DARI, R
在大肠杆菌中，由DNA损伤处理诱导的SOS反应包括两个细胞分裂抑制系统SfiA和SfiC，它们被认为通过与分裂蛋白FtsZ相互作用来阻止细胞分裂。这里显示，SfiA介导的分裂抑制是容易可逆的，即使在没有从头蛋白质合成的情况下，这表明功能性FtsZ分子可以从SfiA-FtsZ复合物中回收。另一方面，SfiC的作用基本上是不可逆的，通过recA（Tif）突变表达诱导60分钟导致分裂抑制，其在诱导期结束后持续至少180分钟。由多拷贝质粒提供的过量的假定靶分子FtsZ抑制SfiA而不是SfiC的作用。SfiA和SfiC的同时诱导导致不可逆的分裂抑制，表明SfiC对SfiA是上位性的。SfiC作用的不可逆性最容易通过假设SfiC产物与SfiA不同是稳定的来解释。SfiA作用的可逆性在lon突变体中较慢，其中SfiA蛋白部分稳定。从分裂恢复的动力学在蛋白质合成的情况下，我们估计的SfiA蛋白的体内半衰期为10分钟的lon+菌株和170分钟的lon突变体。
In Escherichia coli the SOS response, induced by DNA-damaging treatments, includes two systems of cell division inhibition SfiA and SfiC, which are thought to prevent cell division by interacting with the division protein FtsZ. It is shown here that SfiA-mediated division inhibition is readily reversible, even in the absence of de novo protein synthesis, suggesting that functional FtsZ molecules can be recovered from SfiA-FtsZ complexes. The action of SfiC, on the other hand, is essentially irreversible, induction by expression of the recA (Tif) mutation for 60 min results in division inhibition that continues for at least 180 min after the end of the induction period. An excess of the presumed target molecule FtsZ, furnished by a multicopy plasmid, suppresses the action of SfiA but not SfiC. Simultaneous induction of SfiA and SfiC results in irreversible division inhibition, showing that SfiC is epistatic to SfiA. The irreversibility of SfiC action is most readily accounted for by assuming that the SfiC product, unlike SfiA, is stable. The reversibility of SfiA action is slower in a lon mutant, in which the SfiA protein is partially stabilized. From the kinetics of division resumption in the absence of protein synthesis, we estimated the in vivo half-life of the SfiA protein to be 10 min in a lon+ strain and 170 min in a lon mutant.