Affiliation:
1. Biology Department, Princeton University, Princeton, New Jersey
Abstract
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.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
56 articles.
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