Mukherjee A, Cao C, Lutkenhaus J
Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):2885-90. doi: 10.1073/pnas.95.6.2885.
The bacterial cell division protein FtsZ assembles into the cytokinetic Z ring that directs cytokinesis in prokaryotes. In Escherichia coli the formation of the Z ring is prevented by induction of the cell division inhibitor SulA (SfiA), a component of the SOS response. Here we show that a MalE-SulA fusion that retains this inhibitory function in vivo inhibits the GTPase activity and polymerization of FtsZ in vitro. MalE-SulA10, which does not block Z ring formation in vivo, is unable to inhibit the GTPase activity and polymerization in vitro. Furthermore, FtsZ114, which is refractory to SulA in vivo, is not inhibited by MalE-SulA. These results indicate that SulA blocks Z ring formation by blocking FtsZ polymerization.
细菌细胞分裂蛋白FtsZ组装成细胞动力学Z环，该环指导原核生物中的胞质分裂。在大肠杆菌中，细胞分裂抑制剂SulA（SfiA）的诱导可阻止Z环的形成，SulA是SOS反应的一个组成部分。在这里，我们表明，在体内保留这种抑制功能的MalE-SulA融合蛋白在体外抑制FtsZ的GTPase活性和聚合。在体内不阻断Z环形成的MalE-SulA10在体外无法抑制GTPase活性和聚合。此外，在体内对SulA不敏感的FtsZ114不受MalE-SulA的抑制。这些结果表明，SulA通过阻断FtsZ聚合来阻止Z环的形成。
