Linked Life Data

3303332

Source:http://linkedlifedata.com/resource/pubmed/id/3303332

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4817
pubmed:dateCreated
1987-9-23
pubmed:abstractText
Gene expression is dependent on the interaction of DNA binding factors with distinct promoter control elements to activate RNA synthesis. The expression of the HIS4 gene in yeast is under two different control systems. One of these, general amino acid control, involves a DNA binding protein, GCN4, that stimulates transcription in response to amino acid starvation by binding to 5'-TGACTC-3' sequences in the HIS4 promoter region. A second system, the basal level control, stimulates HIS4 transcription in the absence of amino acid starvation. The basal level transcription of the HIS4 gene is under the control of two genes, BAS1 and BAS2, which are also required for the control of purine biosynthesis. In addition, BAS2 is required for the utilization of organic phosphates in the growth medium. Genetic mapping and DNA sequence analysis show that BAS2 is PHO2, a gene previously identified as a regulator of phosphate metabolism. Direct biochemical analysis shows that the BAS2 gene encodes a protein that binds to both the HIS4 and PHO5 promoters. The involvement of a single DNA binding protein in the regulation of histidine, adenine, and phosphate metabolism suggests that yeast may use a few key DNA binding proteins to coordinate the regulation of diverse metabolic pathways.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
237
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
874-80
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Multiple global regulators control HIS4 transcription in yeast.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.