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Altered transcriptional termination in a rifampicin-resistant mutant of Escherichia coli which inhibits the growth of bacteriophage T7

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Summary

A spontaneous rifampicin-resistant mutant of E. coli K 12, RpoB26, which inhibits the growth of bacteriophage T7 has been isolated. The mutation is an RNA polymerase mutation; it also restores the wild-type effect of polar mutations in a rho-deficient strain, probably by restoring transcriptional termination. The efficiency of plating (e.o.p.) of wild-type T7, and of some early region deletion and point mutants of T7 tested, is reduced on RpoB26 by a factor of 10-4. However, some deletion mutants are inhibited more severely (up to 10-7) on RpoB26. We argue that these differences may reflect variations in the frequency of transcriptional termination before gene 1, an essential gene which codes for the T7 RNA polymerase (Summers and Siegel 1970; Chamberlin et al. 1970). We also present data which suggest that the product of a late T7 gene plays a role, by some interaction with the product of gene 1, in the inhibition of T7 in RpoB26. We suggest that different levels of expression of gene 1 may lead to different degrees of inhibition of T7 strains in RpoB26.

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Abbreviations

Gor- :

signifies grow on rif- (Snyder and Montgomery 1974)

Gor- :

strains of T7 are inhibited to the same extent as wild-type T7 on the Rifr mutant RpoB26. The inhibition is relieved by 30 mM NaCl

Gor= :

signifies more severe inhibition than T7 wild-type on RpoB26. This inhibition is relieved by 75 mM NaCl

e.o.p.:

efficiency of plating

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Communicated by E. Bautz

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Schwarz, T.F.R., Yeats, S.M., Connolly, P. et al. Altered transcriptional termination in a rifampicin-resistant mutant of Escherichia coli which inhibits the growth of bacteriophage T7. Molec. Gen. Genet. 183, 181–186 (1981). https://doi.org/10.1007/BF00270159

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