• M Hussain Munavar

      Articles written in Journal of Biosciences

    • Aberrant transcriptionin fit mutants ofEscherichia coli and its alleviation by suppressor mutations

      M Hussain Munavar K Madhavi R Jayaraman

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      Earlier work from this laboratory had identified, mapped and characterised an intragenic suppressor(fitA24) as well as an extragenic suppressor(fitB) for the temperature-sensitive transcription defective mutationfitA76 inEscherichia coli In this communication we report the results of experiments on RNA synthesis and decay of pulse labelled RNA in strains harbouringfit A76,fitB, fitA24, fitA76-fitA24, fitA76-fitB mutation(s) as well as in the isogenicfitA+ fitB+ strain. Taken together with earlier results, this indicates that thefitA andfitB gene products could be involved in the expression of some classes of genes including genes coding for ribosomal proteins. The implications of these results for thein vivo control of transcription inEscherichia coli are discussed.

    • Elucidation of the lesions present in the transcription defectivefitA76 mutant ofEscherichia coli: Implication of phenylalanyl tRNA synthetase subunits as transcription factors

      Sandhya Ramalingam M Hussain Munavar S Sudha A Ruckmani R Jayaraman

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      Earlier reports from our laboratory dealt with the identification, mapping and characterization of a temperature sensitive mutant (fitA76) with a primary transcription defect at 42‡C and two of its suppressors (fitA24 andfitB). We report here the cloning and molecular characterization of a 2-1 kb DNA fragment which complemented the Ts phenotype of thefitA76 andfitA24 mutants but not that due to thefitB mutant. Cloning of this fragment in the T7 expression vector pT7.5 revealed the synthesis of a 33 kDa protein. The fragment hybridized with the Kohara phages 322 and 323 whose overlapping regions includepheS,pheT andrplT genes. Nucleotide sequencing showed that the fragment contains the entirepheS gene and the N-terminal portion ofpheT. Although these results implied that thefitA andpheS genes could be one and the same, earlier data had ruled out such a possibility. In order to know whether thefitA76 mutation defines a novel allele ofpheS, thepheS region of thefitA76 mutant was also sequenced, revealing a G → A nucleotide transition at position 293 of the coding region. This lesion is the same as that reported for thepheS5 mutant. However, it is shown that thefitA76 mutant is primarily transcription-defective while thepheS5 mutant is primarily translation-defective. These results suggested that thefitA76 mutant might harbour another mutation, in addition topheS5. In this report, we present genetic evidence for a second mutation (namedfit95) in thefitA76 mutant. Thefit95 by itself confers a Ts phenotype on rich media devoid of sodium chloride. It is proposed that the subunits of phenylalanyl tRNA synthetase could act as transcription factors (Fit) also.

    • Allele-specific suppression of the temperature sensitivity offitA/fitB mutants ofEscherichia coli by a new mutation (fitC4): Isolation, characterization and its implications in transcription control

      S Vidya B Praveen Kamalakar M Hussain Munavar L Sathish Kumar R Jayaraman

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      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.

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