The cII-independent expression of the phage lambda int gene in RNase III-defective E. coli.
This study compares the rates of lambda protein synthesis after infection of rnc- cells, which are defective in ribonuclease III (RNase III), with the analogous rates in an isogenic rnc+ host. Temporal differences in gene expression are reflected in a delay in turn-off of lambda early proteins as well as in the delayed appearance of late phage functions in rnc- host cells. Moreover, in the two hosts there is a striking difference in the regulation of gene int expression, which in wild-type cells requires the product of the lambda cII (and cIII )genes, whereas Int synthesis occurs in the absence of cII in RNase III-defective cells. These results suggest that RNase III may be a negative regulator of Int synthesis. The expression of int is also shown to be cII- and cIII-independent in rnc+ cells infected with b2-deleted phages, thus confirming previous studies on the negative regulation of int by the b2-region. Possible mechanisms of these two inhibitory effects on int expression are considered and the significance of int regulation in the control of site-specific recombination is discussed.
D010582:Bacteriophage lambda / Q000235:genetics*; D004591:Electrophoresis, Polyacrylamide Gel; D004720:Endonucleases / Q000235:genetics*; D004926:Escherichia coli / Q000235:genetics; D029968:Escherichia coli Proteins; D005814:Genes, Viral; D008242:Lysogeny; D009154:Mutation; D043244:Ribonuclease III; D012260:Ribonucleases / Q000235:genetics*; D014158:Transcription, Genetic; D014764:Viral Proteins / Q000096:biosynthesis
D029968:Escherichia coli Proteins; D014764:Viral Proteins; D004720:Endonucleases; D012260:Ribonucleases; D043244:Ribonuclease III; C468366:ribonuclease III, E coli