GENETIC-EVIDENCE FOR INTERACTION BETWEEN FITA, FITB AND RPOB GENE-PRODUCTS AND ITS IMPLICATION IN TRANSCRIPTION CONTROL IN ESCHERICHIA-COLI

The fitB mutation (Fit, factor involved in transcription) in E. coli w as earlier identified as an extragenic suppressor of the fitA76 mutati on, which confers a temperature-sensitive transcription defect. Here w e show that the fitB mutation by itself confers a temperature-sensitiv e phenotype depending on the presence or absence of NaCl or glucose, o r both, in the medium. The fitB mutation suppresses the temperature-se nsitive phenotype due to the fitA24 mutation also. However, suppressio n of fitA24 by fitB is restricted to rich medium, unlike suppression i n the fitA76 fitB combination where it is independent of the medium. T he strain harbouring fitA76, fitA24 and fitB mutations shows the extra genically suppressed (as in fitA76 fitB) phenotype. Several rif (rpoB) alleles isolated in a fitB genetic background affect growth of the fi tB mutant, depending on the medium of growth, temperature, and presenc e or absence of rifampicin. We propose a model for interaction between fitA and fitB gene products and involvement of the fit genes in trans cription control in vivo.