Role of sulA and sulB in filamentation by lon mutants of Escherichia coli K-12.

TLDR: The simplest model to account for the 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.

Abstract: 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 Images