Scholarlink

Background <p>The <i>fitA</i>/<i>pheS</i> and&#xa0;<i>fitB</i>/<i>pheT</i> genes in <i>E. coli</i> have been proposed to interact with <i>rpoB</i> of RNA polymerase and function as transcription factors. The temperature sensitive (Ts) <i>fitA76</i> mutant harbour two lesions, one in <i>pheS</i> (<i>pheS5</i>) and the other in <i>pheT</i> (<i>fit95</i>). While the <i>pheS5</i> mutant was solely a translation defective, the <i>fitA76</i> mutant with both the mutations (<i>pheS5</i>-<i>fit95</i>) was primarily defective at transcription. Absence of stable RNA detection was considered as the hallmark phenotype of <i>fitA76</i> mutant. In order to elucidate the contribution of <i>fit95</i> in the <i>fitA76</i> mutant, macromolecular defect of <i>fit95</i> mutation alone is studied in this investigation.</p> Methods <p>To detect macromolecular defect, the transcription abnormality of <i>fit95</i> mutant per se was studied via kinetics of decay of pulse labelled RNA.</p> Results <p>Results indicate that <i>fit95</i> is not transcription defective where stable RNA could be detected, similar to <i>pheS5</i> when present alone, indicating that <i>pheS5</i>-<i>fit95</i> interface is essential in eliciting the phenotype characteristic of <i>fitA76.</i> The inferences drawn from these results were implicated with reference to transcription regulation by these Fit factors in vivo are discussed.</p> Conclusion <p>Neither the <i>fit95</i> nor <i>pheS5</i> when present alone was transcription defective per se but in combination (<i>pheS5</i>-<i>fit95</i>) leads to transcription defective in the <i>fitA76</i> mutant.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The pheS5-fit95 interface is essential for eliciting hallmark phenotype of fitA76 in Escherichia coli

  • 期刊论文

  • 发表日期：

    2025年4月30日

查看全文
  • Praveen Belagal

摘要

Background

The fitA/pheS and fitB/pheT genes in E. coli have been proposed to interact with rpoB of RNA polymerase and function as transcription factors. The temperature sensitive (Ts) fitA76 mutant harbour two lesions, one in pheS (pheS5) and the other in pheT (fit95). While the pheS5 mutant was solely a translation defective, the fitA76 mutant with both the mutations (pheS5-fit95) was primarily defective at transcription. Absence of stable RNA detection was considered as the hallmark phenotype of fitA76 mutant. In order to elucidate the contribution of fit95 in the fitA76 mutant, macromolecular defect of fit95 mutation alone is studied in this investigation.

Methods

To detect macromolecular defect, the transcription abnormality of fit95 mutant per se was studied via kinetics of decay of pulse labelled RNA.

Results

Results indicate that fit95 is not transcription defective where stable RNA could be detected, similar to pheS5 when present alone, indicating that pheS5-fit95 interface is essential in eliciting the phenotype characteristic of fitA76. The inferences drawn from these results were implicated with reference to transcription regulation by these Fit factors in vivo are discussed.

Conclusion

Neither the fit95 nor pheS5 when present alone was transcription defective per se but in combination (pheS5-fit95) leads to transcription defective in the fitA76 mutant.