Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-3-11
pubmed:abstractText
The classical, fermentative alcohol dehydrogenase from Saccharomyces cerevisiae, which previously was thought to be constitutive, has been shown to be repressed by growth on nonfermentative carbon sources. The rate of alcohol dehydrogenase I protein synthesis declined 6-fold within 3 to 4 after yeast were transferred from medium containing glucose to medium containing ethanol, and it declined 10-fold after glucose became depleted from the medium during diauxic growth. The decreased rate of alcohol dehydrogenase I protein synthesis was shown not to be the result of an increased rate of degradation of the alcohol dehydrogenase I protein. The decline in alcohol dehydrogenase I protein synthesis was correlated with a 6- to 10-fold decrease in the amount of functional alcohol dehydrogenase I mRNA within 3 to 4 h after transfer from glucose-containing medium to medium containing ethanol. A similar decrease in alcohol dehydrogenase I functional mRNA occurred when cells were depleted of glucose by diauxic growth. Total alcohol dehydrogenase I mRNA, as detected by hybridization to the cloned ADC1 gene, was found in the same relative abundance as the amount of translatable alcohol dehydrogenase I mRNA during the different growth conditions. These results suggest that the alcohol dehydrogenase I protein is transcriptionally regulated.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
258
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1165-71
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
mRNA levels for the fermentative alcohol dehydrogenase of Saccharomyces cerevisiae decrease upon growth on a nonfermentable carbon source.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.