English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

G1 cyclin turnover and nutrient uptake are controlled by a common pathway in yeast

MPS-Authors
/persons/resource/persons289390

Barral,  Y       
Jentsch Group, Friedrich Miescher Laboratory, Max Planck Society;

/persons/resource/persons78165

Jentsch,  S
Jentsch Group, Friedrich Miescher Laboratory, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Barral, Y., Jentsch, S., & Mann, C. (1995). G1 cyclin turnover and nutrient uptake are controlled by a common pathway in yeast. Genes and Development, 9(4), 399-409. doi:10.1101/gad.9.4.399.


Cite as: https://hdl.handle.net/21.11116/0000-000D-137E-1
Abstract
Entry into a new cell cycle is triggered by environmental signals at a point called Start in G1 phase. A key regulator of this transition step in yeast is the CDC28 kinase together with its short-lived regulatory subunits called G1-cyclins or CLN proteins. To identify genes involved in G1-cyclin degradation, we employed a genetic screen by selecting for stable CLN1-beta-galactosidase fusion proteins. Surprisingly, one group of mutants was found to be allelic to GRR1, a gene previously described to be involved in glucose uptake, glucose repression, and divalent cation transport. In grr1 mutants, both CLN1 and CLN2 cyclins are significantly stabilized. A suppressor analysis indicated that G1-cyclin stabilization in grr1 was not a consequence of the nutrient uptake defect. This suggests that the GRR1 gene product is part of a common regulatory pathway linking two functions important for cell growth, nutrient uptake, and G1 cyclin-controlled cell division.