Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

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

MPG-Autoren
/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;

Externe Ressourcen
Es sind keine externen Ressourcen hinterlegt
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

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.


Zitierlink: https://hdl.handle.net/21.11116/0000-000D-137E-1
Zusammenfassung
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.