Transcription-Defective soxR Mutants of Escherichia coli: Isolation and In Vivo Characterization
AUTOR(ES)
Chander, Monica
FONTE
American Society for Microbiology
RESUMO
The soxRS regulon protects Escherichia coli from superoxide and nitric oxide stress. SoxR protein, a transcription factor that senses oxidative stress via its [2Fe-2S] centers, transduces the signal to the soxS promoter to stimulate RNA polymerase. Here we describe 29 mutant alleles of soxR that cause defects in the activation of soxS transcription in response to paraquat, a superoxide stress agent. Owing to the selection and screen used in their isolation, most of these mutant alleles encode proteins that retained specific binding activity for the soxS promoter in vivo. The mutations were found throughout the SoxR polypeptide, although those closer to the N terminus typically exhibited greater defects in DNA binding. The degree of the defect in the transcriptional response to superoxide caused by each mutation was closely paralleled by its impaired response to nitric oxide. This work begins the general identification of the residues in the SoxR polypeptide that are critical for transducing oxidative stress signals into gene activation.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=152623Documentos Relacionados
- A reducing system of the superoxide sensor SoxR in Escherichia coli
- Two divergently transcribed genes, soxR and soxS, control a superoxide response regulon of Escherichia coli.
- Isolation and characterization of conditional lethal mutants of Escherichia coli defective in transcription termination factor rho.
- Oxygen, iron, carbon, and superoxide control of the fumarase fumA and fumC genes of Escherichia coli: role of the arcA, fnr, and soxR gene products.
- soxR, a locus governing a superoxide response regulon in Escherichia coli K-12.