Genetic evidence for interaction between fitA, fitB and rpoB gene products and its implication in transcription control in Escherichia coli

Abstract

The fitB mutation (Fit, factor involved in transcription) inE. coli was earlier identified as an extragenic suppressor of thefitA76 mutation, which confers a temperature sensitive transcription defect. Here we show that the fitB mutation by itself confers a temperature-sensitive phenotype depending on the presence or absence of NaCl or glucose, or both, in the medium. The fitB mutation suppresses the temperature-sensitive phenotype due to thefitA24 mutation also. However, suppression off it A24 byfit B is restricted to rich medium, unlike suppression in thefitA76 fitB combination where it is independent of the medium. The strain harbouringfitA76, fitA24 andfitB mutations shows the extragenically suppressed (as infit A76 fit B) phenotype. Severalrif (rpoB) alleles isolated in afitB genetic background affect growth of thefit B mutant, depending on the medium of growth, temperature, and presence or absence of rifampicin. We propose a model for interaction betweenfitA andfitB gene products and involvement of thefit genes in transcription controlin vivo.