Mutations ts2158 and ts1882, which confer temperature sensitivity of septum formation, map near leu in the region of min 2.0 to 2.1 on the Escherichia coli chromosome. These mutants stop division abruptly and grow as filaments at 42 C; when returned to 28 C, division resumes after about 30 min to produce short cells. The product of the gene defined by these mutations probably is required during all stages of septum formation rather than specifically for initiation of septation. Filaments that formed at 42 C contained incomplete constrictions (septa). When actively dividing filaments (i.e., those incubated at 28 C until division resumed) were shifted to 42 C a second time, division again stopped abruptly and incomplete constrictions persisted during the incubation at 42 C. Filaments that were subjected to 28 C incubation for a brief time (10, 20, or 30 min) before being shifted again to 42 C did not resume division as would be expected of a strain defective in initiating septation. Mutations ts1882 and ts2158 are recessive to the ts+ allele, which is consistent with the interpretation that these mutations cause the loss of a function. They did not complement each other and presumably represent one cistron. Mutants carrying ts1882 and ts2158 mutations were compared with a mutant defective in the ftsA allele, also known to map near leu.

The Escherichia coli mutations ts1882 and ts2158 cause temperature-sensitive septum formation and result in growth of cells as long, multinucleate, nonseptate filaments at 42 C. When filaments are transferred to 28 C, they divide into short cells. Chloramphenicol, when added to cultures of filaments at the time of' temperature reduction, inhibited division of filaments when these temperaturesensitive mutations were present in the K-12 strain AB1157. However, when the ts1882 and ts2158 mutations were present in another K-12 strain, UTH4113, filaments of these strains divided in the presence of chloramphenicol.