Maguin E, Lutkenhaus J, D'Ari R
J Bacteriol. 1986 Jun;166(3):733-8. doi: 10.1128/jb.166.3.733-738.1986.
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.
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,即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。本文表明,即使在没有从头合成蛋白质的情况下,SfiA介导的分裂抑制也很容易逆转,这表明功能性FtsZ分子可以从SfiA - FtsZ复合物中恢复。另一方面,SfiC的作用基本上是不可逆的;recA(Tif)突变体表达60分钟诱导产生的分裂抑制在诱导期结束后至少持续180分钟。多拷贝质粒提供的过量假定靶分子FtsZ可抑制SfiA的作用,但不能抑制SfiC的作用。同时诱导SfiA和SfiC会导致不可逆的分裂抑制,表明SfiC对SfiA呈上位性。假设SfiC产物与SfiA不同,是稳定的,那么SfiC作用的不可逆性就很容易解释了。在lon突变体中,SfiA作用的可逆性较慢;在lon突变体中,SfiA蛋白部分稳定。根据无蛋白质合成时分裂恢复的动力学,我们估计在lon +菌株中SfiA蛋白的体内半衰期为10分钟,在lon突变体中为170分钟。