IDENTIFICATION OF A NEW INHIBITOR OF ESSENTIAL DIVISION GENE FTSZ AS THE KIL GENE OF DEFECTIVE PROPHAGE RAC

Citation
A. Conter et al., IDENTIFICATION OF A NEW INHIBITOR OF ESSENTIAL DIVISION GENE FTSZ AS THE KIL GENE OF DEFECTIVE PROPHAGE RAC, Journal of bacteriology, 178(17), 1996, pp. 5100-5104
Citations number
26
Categorie Soggetti
Microbiology
Journal title
ISSN journal
00219193
Volume
178
Issue
17
Year of publication
1996
Pages
5100 - 5104
Database
ISI
SICI code
0021-9193(1996)178:17<5100:IOANIO>2.0.ZU;2-Q
Abstract
A gene function carried by a plasmid, causing arrest of cell division in Escherichia coli, has been identified as the product of a short ope n reading frame of the prophage Rac, previously designated orfE, expre ssed only under conditions of prophage induction. Because Rac carries a killing function expressed under conditions of zygotic induction, an orfE-defective Rac(+) strain was constructed. This strain had lost th e killing function, indicating that orfE is kil. Division inhibition b y kil was specifically relieved by overexpression of essential divisio n gene ftsZ. The kil gene product acts independently of the min operon , and its effects are increased in conditions of high cyclic AMP (cAMP ) receptor protein-cAMP complex levels in the cell. Furthermore, at hi gh levels of expression, kil product distorts the rod shape of the cel ls. These features distinguish kil-encoded protein from the inhibitory product of gene dicB, which occupies a similar genetic location in Ki m (Qin), another defective prophage of Escherichia coli.