Linked Life Data

8052232

Source:http://linkedlifedata.com/resource/pubmed/id/8052232

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-9-2
pubmed:abstractText
The glucose kinase gene (glkA-ORF3) of Streptomyces coelicolor A3(2) plays an essential role in glucose utilisation and in glucose repression of a variety of genes involved in the utilisation of alternative carbon sources. These genes include dagA, which encodes an extracellular agarase that permits agar utilisation. Suppressor mutants of glkA-ORF3 deletion strains capable of utilising glucose (Glc+) arise at a frequency of about 10(-5) on prolonged incubation. The Glc+ phenotype of the mutants is reversible (at a frequency of about 10(-3) and reflects either the activation of a normally silent glucose kinase gene or the modification of an existing sugar kinase. Although the level of glucose kinase activity in the Glc+ supressor mutants is similar to that in the glkA+ parental strain, glucose repression of dagA remains defective. Expression of the glucose kinase gene of Zymomonas mobilis in glkA-ORF3 mutants restored glucose utilisation, but not glucose repression of dagA. Over-expression of glkA-ORF3 on a high-copy-number plasmid failed to restore glucose repression of dagA in glkA-ORF3 mutants and led to loss of glucose repression of dagA in a glkA+ strain. These results suggest that glucose phosphorylation itself is not sufficient for glucose repression and that glkA-ORF3 plays a specific regulatory role in triggering glucose repression in S. coelicolor A3(2).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0026-8925
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
244
pubmed:geneSymbol
dagA
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
135-43
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Glucose repression in Streptomyces coelicolor A3(2): a likely regulatory role for glucose kinase.
pubmed:affiliation
John Innes Centre, Colney, Norwich, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't