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pubmed:abstractText |
The lon(-) mutation is responsible for a defect in cell division of Escherichia coli lightly irradiated with ultraviolet light (UV). These lon(-) mutants can be isolated readily by a procedure described here. Physiological studies were performed with the objective of determining the role of the lon gene. Unirradiated lon(-) mutants grow normally, except that a correlation of this mutation with capsule formation has been noted previously. These two properties can be separated, however. After irradiation, lon(-) grows as long filaments because septum formation is prevented. The filaments eventually lyse. Mass increase and deoxyribonucleic acid and enzyme synthesis appear to proceed normally. Thus, the lesion produced by UV appears to be highly specific. In bacteria that carry both genes (merozygotes), lon(+) is dominant to lon(-). Septum formation is restored to irradiated lon(-) bacteria by introduction of lon(+) by conjugation. Also, normal growth can be restored by nutritional variations. It is concluded that lon(+) is able to nullify the effects of the UV lesion under conditions where lon(-) cannot. Possibly, capsule precursors that can accumulate in the latter are responsible for the difference because they interfere with repair of the UV lesion.
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