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Regulation of the Cln3–Cdc28 kinase by cAMP in Saccharomyces cerevisiae
Author(s) -
Hall Duane D.,
Markwardt David D.,
Parviz Fereshteh,
Heideman Warren
Publication year - 1998
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/17.15.4370
Subject(s) - biology , saccharomyces cerevisiae , cyclin dependent kinase 1 , yeast , protein kinase a , cell cycle , microbiology and biotechnology , kinase , transcriptional regulation , transcription factor , biochemistry , cell , gene
The yeast Saccharomyces cerevisiae grows at widely varying rates in different growth media. In order to maintain a relatively constant cell size, yeast cells must regulate the rate of progress through the cell cycle to match changes in growth rate, moving quickly through G 1 in rich medium, and slowly in poor medium. We have examined connections between nutrients, and the expression and activity of Cln3–Cdc28 kinase that regulates the G 1 –S boundary of the cell cycle in yeast, a point referred to as Start. We find that Cln3 protein levels are highest in glucose and lower in poorer carbon sources. This regulation involves both transcriptional and post‐transcriptional control. Although the Ras–cAMP pathway does not appear to affect CLN3 transcription, cAMP increases Cln3 protein levels and Cln3–Cdc28 kinase activity. This regulation requires untranslated regions of the CLN3 message, and can be explained by changes in protein synthesis rates caused by cAMP. A model for CLN3 regulation and function is presented in which CLN3 regulates G 1 length in response to nutrients.