The temperature sensitive transcription defective mutant ofEscherichia coli originallycalled fitA76 has been shown to harbour two missense mutations namelypheS5 andfit95. In order to obtain a suppressor offitA76, possibly mapping inrpoD locus, a Ts+ derivative (JV4) was isolated from afitA76 mutant. It was found that JV4 neither harbours the lesions present in the originalfitA 76 nor a suppressor that maps in or nearrpoD. We show that JV4 harbours a modified form offitA76 (designatedfitA76*) together with its suppressor. The results presented here indicate that thefit95 lesion is intact in thefitA 76* mutant and the modification should be at the positionof pheS5. Based on the cotransduction of the suppressor mutation and/or its wild type allelewith pps, aroD andzdj-3124::Tn10 kan we have mapped its location to 39.01 min on theE. coli chromosome. We tentatively designate the locus defined by this new extragenic suppressoras fitC and the suppressor allele asfitC4. While fitC4 could suppress the Ts phenotype offitA76* present in JV4, it fails to suppress the Ts phenotype of theoriginal fitA76 mutant (harbouringpheS5 andfit95). AlsofitC4 could suppress the Ts phenotype of a strain harbouringonly pheS5. Interestingly, thefitC4 Ts phenotype could also be suppressed byfit95. The pattern of decay of pulse labelled RNA in the strains harbouringfitC4 and thefitA76* resembles that of theoriginal fitA76 mutant implying a transcription defect similar to that offitA76 in both these mutants. The implications of these findings with special reference to transcription control by Fit factorsin vivo are discussed.