Celis containing the pleiotropic Escherichia coli mutation ion 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 Ion strains but do not affect the mucoidal or degradation defect of these strains. An isogenic set of strains carrying combinations of Ion, suA, and sulB was constructed, and their behavior during normal growth and after ultraviolet treatment was studied. suA mutations had no detectable phenotype in Ion+' cells; the Ion suA 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 Ion and suA. 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 Ion participate in a pathway of filamentation independent of that which produces transient filamentation in wild-type strains; sulB product may be the target of suA action and may play a role in normal cell division.

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