Role of sulA and sulB in filamentation by lon mutants of Escherichia coli K-12.
AUTOR(ES)
Gottesman, S
RESUMO
Cells containing the pleiotropic Escherichia coli mutation lon filament extensively and die after exposure to ultraviolet light. Outside suppressors of the ultraviolet sensitivity, called sul, have previously been described at two loci; these mutations reverse the ultraviolet sensitivity of lon strains but do not affect the mucoidal or degradation defect of these strains. An isogenic set of strains carrying combinations of lon, sulA, and sulI was constructed, and their behavior during normal growth and after ultraviolet treatment was studied. sulA mutations had no detectable phenotype in lon+ cells; the lon sulA strains filamented transiently after ultraviolet irradiation, as did lon+ sul+ cells. We found that the sulB mutation, which alters cell morphology and slows recovery from transient filamentation after ultraviolet treatment, was epistatic to both lon and sulA. Whereas sulA mutations were recessive to the wild-type allele, sulB was partially dominant. The simplest model to account for our observations is that sulA and lon participate in a pathway of filamentation independent of that which produces transient filamentation in wild-type strains; sulB product may be the target of sulA action and may play a role in normal cell division.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=216189Documentos Relacionados
- Role of the SulB (FtsZ) protein in division inhibition during the SOS response in Escherichia coli: FtsZ stabilizes the inhibitor SulA in maxicells.
- Proteolysis and modulation of the activity of the cell division inhibitor SulA in Escherichia coli lon mutants.
- Gene lon and plasmid inheritance in Escherichia coli K-12.
- Regulation of cell division in Escherichia coli: SOS induction and cellular location of the sulA protein, a key to lon-associated filamentation and death.
- Iron uptake in colicin B-resistant mutants of Escherichia coli K-12.