Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-9-18
pubmed:abstractText
The Saccharomyces cerevisiae ALG7 gene, which functions by initiating the dolichol pathway of protein N-glycosylation, displays properties of an early growth-response gene. To initiate studies of the involvement of ALG7 in cellular proliferation, we have now more precisely analyzed ALG7 expression in the G1 phase of cell cycle. We show that the rapid rate of ALG7 mRNA accumulation following growth stimulation was attenuated soon thereafter and that ALG7 growth induction occurred irrespective of alpha-factor. ALG7 growth induction was observed in mutants conditionally defective for reentry into the cell cycle from the stationary phase, indicating that the induction occurred prior to the performance of START. In addition, the steady-state levels of ALG7 mRNAs declined four-fold in response to START-I cell division arrest brought about by alpha-factor treatment later in G1. Importantly, deregulated expression of ALG7 resulted in an aberrant alpha-factor response. Our data not only indicate that ALG7 expression is regulated at two critical control points in G1 that determine the proliferative potential of cells, but also provide a link between ALG7 and START.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-4827
pubmed:author
pubmed:issnType
Print
pubmed:volume
219
pubmed:geneSymbol
ALG7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
477-86
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Expression of the first N-glycosylation gene in the dolichol pathway, ALG7, is regulated at two major control points in the G1 phase of the Saccharomyces cerevisiae cell cycle.
pubmed:affiliation
Department of Oral Biology, Boston University Medical Center, Massachusetts 02118, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.