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OsnR is an autoregulatory negative transcription factor controlling redox-dependent stress responses in Corynebacterium glutamicum

Authors
Jeong, HaeriKim, YounheeLee, Heung-Shick
Issue Date
18-10월-2021
Publisher
BMC
Keywords
Corynebacterium glutamicum; Oxidative stress; osnR; sigH
Citation
MICROBIAL CELL FACTORIES, v.20, no.1
Indexed
SCIE
SCOPUS
Journal Title
MICROBIAL CELL FACTORIES
Volume
20
Number
1
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/136034
DOI
10.1186/s12934-021-01693-1
ISSN
1475-2859
Abstract
Background Corynebacterium glutamicum is used in the industrial production of amino acids and nucleotides. During the course of fermentation, C. glutamicum cells face various stresses and employ multiple regulatory genes to cope with the oxidative stress. The osnR gene plays a negative regulatory role in redox-dependent oxidative-stress responses, but the underlying mechanism is not known yet. Results Overexpression of the osnR gene in C. glutamicum affected the expression of genes involved in the mycothiol metabolism. ChIP-seq analysis revealed that OsnR binds to the promoter region of multiple genes, including osnR and cg0026, which seems to function in the membrane-associated redox metabolism. Studies on the role of the osnR gene involving in vitro assays employing purified OsnR proteins and in vivo physiological analyses have identified that OsnR inhibits the transcription of its own gene. Further, oxidant diamide stimulates OsnR-binding to the promoter region of the osnR gene. The genes affected by the overexpression of osnR have been found to be under the control of sigma(H). In the osnR-overexpressing strain, the transcription of sigH is significantly decreased and the stimulation of sigH transcription by external stress is lost, suggesting that osnR and sigH form an intimate regulatory network. Conclusions Our study suggests that OsnR not only functions as a transcriptional repressor of its own gene and of those involved in redox-dependent stress responses but also participates in the global transcriptional regulation by controlling the transcription of other master regulators, such as sigH.
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