Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23
pubmed:dateCreated
1991-12-26
pubmed:abstractText
The transcription from the spoVG promoter of Bacillus subtilis is induced at the start of the stationary phase of growth and is dependent on the expression of the spoOA, spoOB, and spoOH genes. It is repressed in cells grown in the presence of excess glucose and glutamine and is under the negative control of the abrB gene. The spoOA and spoOB gene products function to suppress the negative control exerted by abrB. Transcription initiation requires the form of RNA polymerase holoenzyme that contains the spoOH gene product, sigma H. Optimal transcription also requires an upstream A-T-rich region termed the upstream activating sequence (UAS). The mechanism of UAS function was examined through mutational analysis of the spoVG promoter region. Deletion of the UAS or positioning the UAS one half turn or one full turn of the DNA helix upstream of its location in wild-type spoVG resulted in a severe reduction in promoter activity. Deletion of most of the UAS abolished the abrB-dependent repression of spoVG transcription. Higher activity was observed when the UAS was inserted 10 bp (one turn of the helix) upstream than when the sequence was repositioned either 5 or 13 bp upstream. Sequences upstream of the UAS were found not to be involved with the position-dependent function of the UAS. Positioning the UAS 42 or 116 bp upstream eliminated the stimulatory effect of the sequence on spoVG transcription. These data indicate that the UAS functions effectively when it is in close proximity to the -35 region. In vitro transcription analysis indicated that the deletion and insertion mutation affecting the UAS impair RNA polymerase-spoVG promoter interaction. Deletion of the UAS showed that the negative effect of exogenous glucose and glutamine is not dependent on the UAS but is exerted at a site within or near the -35 and -10 regions.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-12736, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-1651394, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-1850083, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-1870123, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-1904128, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-1906866, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2105305, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2118512, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2122453, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2416474, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2437099, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2500529, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2504584, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2509422, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2509423, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2512122, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2540150, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2543669, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2554317, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2690009, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2694932, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2848009, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-2981756, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-3057439, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-3099284, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-3277943, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-4956288, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-6350894, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-6405278, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-6411929, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-6414720, http://linkedlifedata.com/resource/pubmed/commentcorrection/1938951-6790515
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9193
pubmed:author
pubmed:issnType
Print
pubmed:volume
173
pubmed:geneSymbol
spoOA, spoOH, spoVG
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7557-64
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:1938951-Bacillus subtilis, pubmed-meshheading:1938951-Base Sequence, pubmed-meshheading:1938951-Carbon, pubmed-meshheading:1938951-Chromosome Deletion, pubmed-meshheading:1938951-DNA, Bacterial, pubmed-meshheading:1938951-DNA-Directed RNA Polymerases, pubmed-meshheading:1938951-Gene Expression Regulation, Bacterial, pubmed-meshheading:1938951-Genes, Bacterial, pubmed-meshheading:1938951-Glucose, pubmed-meshheading:1938951-Glutamine, pubmed-meshheading:1938951-Kinetics, pubmed-meshheading:1938951-Molecular Sequence Data, pubmed-meshheading:1938951-Mutagenesis, Site-Directed, pubmed-meshheading:1938951-Nitrogen, pubmed-meshheading:1938951-Promoter Regions, Genetic, pubmed-meshheading:1938951-Sigma Factor, pubmed-meshheading:1938951-Spores, Bacterial, pubmed-meshheading:1938951-Transcription, Genetic, pubmed-meshheading:1938951-beta-Galactosidase
pubmed:year
1991
pubmed:articleTitle
Analysis of the upstream activating sequence and site of carbon and nitrogen source repression in the promoter of an early-induced sporulation gene of Bacillus subtilis.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, Shreveport 71130.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.