a Department of Microbiology, The University of Texas at Austin, Texas 78712
ABSTRACT
The lon mutants of Escherichia coli grow apparently normally except that, after temporary periods of inhibition of deoxyribonucleic acid synthesis, septum formation is specifically inhibited. Under these conditions, long, multinucleate, nonseptate filaments result. The lon mutation also creates a defect such that wild-type bacteriophage
fails to lysogenize lon mutants efficiently and consequently forms clear plaques on a lon host. Two lines of evidence suggest that this failure probably results from interference with expression of the
cI gene, which codes for repressor, or with repressor action:-(i) when a lon mutant was infected with a
cII, cIII, or c Y mutant, there was an additive effect between the lon mutation and the
c mutations upon reduction of lysogenization frequency; and (ii) lon mutants permitted the growth of the
cro mutant under conditions in which the repressor was active. The isolation of
mutants (
tp) which gained the ability to form turbid plaques on lon cells is also reported.
1 Present address: Chemistry Department, Harvard University, Cambridge, Mass. 02138, on leave from the University of Texas at Austin.
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
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