Pogliano J, Dong J M, De Wulf P, Furlong D, Boyd D, Losick R, Pogliano K, Lin E C
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Bacteriol. 1998 Jul;180(13):3486-90. doi: 10.1128/JB.180.13.3486-3490.1998.
In Escherichia coli, certain mutations in the cpxA gene (encoding a sensor kinase of a two-component signal transduction system) randomize the location of FtsZ ring assembly and dramatically affect cell division. However, deletion of the cpxRA operon, encoding the sensor kinase and its cognate regulator CpxR, has no effect on division site biogenesis. It appears that certain mutant sensor kinases (CpxA*) either exhibit hyperactivity on CpxR or extend their signalling activity to one or more noncognate response regulators involved in cell division.
在大肠杆菌中,cpxA基因(编码双组分信号转导系统的传感激酶)的某些突变会使FtsZ环组装的位置随机化,并显著影响细胞分裂。然而,编码传感激酶及其同源调节因子CpxR的cpxRA操纵子的缺失对分裂位点的生物发生没有影响。似乎某些突变的传感激酶(CpxA*)要么对CpxR表现出过度活性,要么将其信号传导活性扩展到参与细胞分裂的一个或多个非同源反应调节因子。