Analysis of tnrA alleles which result in a glucose-resistant sporulation phenotype in Bacillus subtilis

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dc.contributor.authorByung Sik Shin-
dc.contributor.authorSoo Keun Choi-
dc.contributor.authorIssar Smith-
dc.contributor.authorSeung Hwan Park-
dc.date.accessioned2017-04-19T08:57:10Z-
dc.date.available2017-04-19T08:57:10Z-
dc.date.issued2000-
dc.identifier.issn0021-9193-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/5136-
dc.description.abstractBacillus subtilis cells cannot sporulate in the presence of catabolites such as glucose. During the analysis of Tn10-generated mutants, we found that deletion of the C-terminal region of the tnrA gene, which encodes a global regulator that positively regulates a number of genes in response to nitrogen limitation, results in a catabolite-resistant sporulation phenotype. Analyses of nrg-lacZ and nasB-lacZ, which are activated by TnrA under nitrogen limitation, showed that C-terminally truncated TnrA activates nitrogen-regulated genes constitutively. The relief of catabolite repression of sporulation may result from the uncontrolled expression of the TnrA-regulated genes.-
dc.publisherAmer Soc Microb-
dc.titleAnalysis of tnrA alleles which result in a glucose-resistant sporulation phenotype in Bacillus subtilis-
dc.title.alternativeAnalysis of tnrA alleles which result in a glucose-resistant sporulation phenotype in Bacillus subtilis-
dc.typeArticle-
dc.citation.titleJournal of Bacteriology-
dc.citation.number17-
dc.citation.endPage5012-
dc.citation.startPage5009-
dc.citation.volume182-
dc.contributor.affiliatedAuthorSoo Keun Choi-
dc.contributor.affiliatedAuthorSeung Hwan Park-
dc.contributor.alternativeName신병식-
dc.contributor.alternativeName최수근-
dc.contributor.alternativeNameSmith-
dc.contributor.alternativeName박승환-
dc.identifier.bibliographicCitationJournal of Bacteriology, vol. 182, no. 17, pp. 5009-5012-
dc.identifier.doi10.1128/JB.182.17.5009-5012.2000-
dc.description.journalClassY-
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Division of Research on National Challenges > Infectious Disease Research Center > 1. Journal Articles
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