Affiliation:
1. Department of Microbiology, University of Connecticut Health Center, Farmington 06032.
Abstract
Mutation of Escherichia coli minicell locus (minB) results in aberrant placement of the division septum. In this paper we report the isolation and characterization of the minB locus. Replacement of the chromosomal minB+ allele by cloned minB sequences containing transposon insertions resulted in the minicell phenotype, indicating that minB+ function is required to maintain the normal division pattern. Paradoxically, overexpression of the locus also resulted in the minicell phenotype. The locus codes for several peptides whose expression is coordinately affected by transposon mutations that also eliminate minB+ function. A subset of the minB peptides is sufficient to prevent minicell formation in minB1 mutants or to induce minicell formation when overproduced in wild-type strains, implicating these peptides in the normal process of localization of the division site. The results indicate that minB is a complex locus whose expression must be maintained within certain limits to maintain the normal pattern of localization of the division septum.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Reference27 articles.
1. Miniature Escherichia coli cells deficient in DNA;Adler H. I.;Proc. Natl. Acad. Sci. USA,1967
2. Linkage map of Escherichia coli K-12, edition 7;Bachmann B. J.;Microbiol. Rev.,1983
3. Boulnois G. J. and K. N. Timmnis. 1984. Synthesis of plasmidencoded polypeptides in maxicells p. 204-211. In A. Puhler and K. N. Timmis (ed.) Advanced molecular genetics. Springer-Verlag Berlin.
4. The SPT6 gene is essential for growth and is required for 8-mediated transcription in Saccharomyces cerevisiae;Clark-Adams C. D.;Mol. Cell. Biol.,1987
5. Compartmentalization of the periplasmic space at division sites in gram-negative bacteria;Cook W. R.;J. Bacteriol.,1986
Cited by
130 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献