Literature DB >> 22573149

Negative role of wblA in response to oxidative stress in Streptomyces coelicolor.

Jin-Su Kim1, Han-Na Lee, Pil Kim, Heung-Shick Lee, Eung-Soo Kim.   

Abstract

In this study, we analyzed the oxidative stress response of wblA (whiB-like gene A, SCO3579), which was previously shown to be a global antibiotic down-regulator in Streptomyces coelicolor. Ever since a WblA ortholog named WhcA in Corynebacterium glutamicum was found to play a negative role in the oxidative stress response, S. coelicolor wblA has been proposed to have a similar effect. A wblA-deletion mutant exhibited a less sensitive response to oxidative stress induced by diamide present in solid plate culture. Using real-time RT-PCR analysis, we also compared the transcription levels of oxidative stress-related genes, including sodF, sodF2, sodN, trxB, and trxB2, between S. coelicolor wild type and a wblA-deletion mutant in the presence or absence of oxidative stress. Target genes were expressed higher in the wblA-deletion mutant compared with wild type, both in the absence and presence of oxidative stress. Moreover, expression of these target genes in S. coelicolor wild type was stimulated only in the presence of oxidative stress, suggesting that WblA plays a negative role in the oxidative stress response of S. coelicolor, similar to that of C. glutamicum WhcA, through the transcriptional regulation of oxidative stress-related genes.

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Year:  2012        PMID: 22573149     DOI: 10.4014/jmb.1112.12032

Source DB:  PubMed          Journal:  J Microbiol Biotechnol        ISSN: 1017-7825            Impact factor:   2.351


  11 in total

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Journal:  Appl Environ Microbiol       Date:  2013-04-19       Impact factor: 4.792

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Journal:  Appl Environ Microbiol       Date:  2021-10-20       Impact factor: 4.792

9.  Identification and biotechnological application of novel regulatory genes involved in Streptomyces polyketide overproduction through reverse engineering strategy.

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10.  Rational engineering of Streptomyces albus J1074 for the overexpression of secondary metabolite gene clusters.

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