Analysis of ftsZ mutations that confer resistance to the cell division inhibitor SulA (SfiA)
- PMID: 2145263
- PMCID: PMC526871
- DOI: 10.1128/jb.172.10.5602-5609.1990
Analysis of ftsZ mutations that confer resistance to the cell division inhibitor SulA (SfiA)
Abstract
In Escherichia coli, the ftsZ gene is thought to be an essential cell division gene. Several dominant mutations that make lon mutant cells refractory to the cell division inhibitor SulA, sulB9, sulB25, and sfiB114, have been mapped to the ftsZ gene. DNA sequence analysis of these mutations and the sfiB103 mutation confirmed that all of these mutations mapped within the ftsZ gene and revealed that the two sulB mutations were identical and by selection for resistance to higher levels of SulA, contained a second mutation within the ftsZ gene. We therefore propose that these mutations be redesignated ftsZ(Rsa) for resistance to SulA. A procedure involving mutagenesis of ftsZ cloned on low-copy-number vectors was used to isolate three additional ftsZ(Rsa) mutations. DNA sequence analysis of these mutations revealed that they were distinct from the previously isolated mutations. One of these mutations, ftsZ3(Rsa), led to an altered FtsZ protein that could no longer support cell growth but still conferred the Rsa phenotype in the presence of ftsZ+. In addition to being resistant to SulA, all ftsZ(Rsa) mutations also conferred resistance to a LacZ-FtsZ hybrid protein (ZZ). One possibility is that FtsZ functions as a multimer and that FtsZ(Rsa) mutant proteins have an increased ability for multimerization, making them resistant to SulA and ZZ.
Similar articles
-
Role of the SulB (FtsZ) protein in division inhibition during the SOS response in Escherichia coli: FtsZ stabilizes the inhibitor SulA in maxicells.Proc Natl Acad Sci U S A. 1985 Sep;82(18):6045-9. doi: 10.1073/pnas.82.18.6045. Proc Natl Acad Sci U S A. 1985. PMID: 2994059 Free PMC article.
-
Coupling of DNA replication and cell division: sulB is an allele of ftsZ.J Bacteriol. 1983 Jun;154(3):1339-46. doi: 10.1128/jb.154.3.1339-1346.1983. J Bacteriol. 1983. PMID: 6343351 Free PMC article.
-
A lacZ-ftsZ gene fusion is an analog of the cell division inhibitor sulA.J Bacteriol. 1984 Mar;157(3):815-20. doi: 10.1128/jb.157.3.815-820.1984. J Bacteriol. 1984. PMID: 6230346 Free PMC article.
-
Mutations in ftsZ that confer resistance to SulA affect the interaction of FtsZ with GTP.J Bacteriol. 1994 Jan;176(1):130-6. doi: 10.1128/jb.176.1.130-136.1994. J Bacteriol. 1994. PMID: 8282688 Free PMC article.
-
Interaction between the min locus and ftsZ.J Bacteriol. 1990 Oct;172(10):5610-6. doi: 10.1128/jb.172.10.5610-5616.1990. J Bacteriol. 1990. PMID: 2211499 Free PMC article.
Cited by
-
Effects of mutations involving cell division, recombination, and chromosome dimer resolution on a priA2::kan mutant.Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8203-10. doi: 10.1073/pnas.121007698. Proc Natl Acad Sci U S A. 2001. PMID: 11459954 Free PMC article.
-
Crystal structure of the SOS cell division inhibitor SulA and in complex with FtsZ.Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7889-94. doi: 10.1073/pnas.1330742100. Epub 2003 Jun 13. Proc Natl Acad Sci U S A. 2003. PMID: 12808143 Free PMC article.
-
A replication-inhibited unsegregated nucleoid at mid-cell blocks Z-ring formation and cell division independently of SOS and the SlmA nucleoid occlusion protein in Escherichia coli.J Bacteriol. 2014 Jan;196(1):36-49. doi: 10.1128/JB.01230-12. Epub 2013 Oct 18. J Bacteriol. 2014. PMID: 24142249 Free PMC article.
-
Selective alleviation of Mitomycin C sensitivity in lexA3 strains of Escherichia coli demands allele specificity of rif-nal mutations: a pivotal role for rpoB87-gyrA87 mutations.PLoS One. 2014 Feb 3;9(2):e87702. doi: 10.1371/journal.pone.0087702. eCollection 2014. PLoS One. 2014. PMID: 24498357 Free PMC article.
-
Substrate sequestration by a proteolytically inactive Lon mutant.Proc Natl Acad Sci U S A. 1999 May 25;96(11):6064-71. doi: 10.1073/pnas.96.11.6064. Proc Natl Acad Sci U S A. 1999. PMID: 10339542 Free PMC article.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases