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Deregulation of CLN 1 and CLN 2 in the Saccharomyces cerevisiae whi2 Mutant
Author(s) -
RADCLIFFE PIPPA,
TREVETHICK JANET,
TYERS MIKE,
SUDBERY PETER
Publication year - 1997
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/(sici)1097-0061(19970630)13:8<707::aid-yea130>3.0.co;2-9
Subject(s) - biology , ectopic expression , mutant , cyclin , microbiology and biotechnology , saccharomyces cerevisiae , cell cycle checkpoint , wild type , cell cycle , mutation , gene , genetics
Wild‐type cells of the budding yeast Saccharomyces cerevisiae arrest in G1 upon nutrient exhaustion. Cell cycle arrest requires the WHI2 gene since whi2 mutants continue to divide and become abnormally small as nutrients are depleted. Here we show that CLN 1 and CLN 2 transcript levels in a whi2 strain are higher during exponential growth, and persist longer upon starvation, than in an isogenic wild‐type strain. In contrast to CLN 1 and CLN 2, CLN 3 levels declined only at very high cell density and were unaffected by the whi2 mutation. Elevated CLN expression is sufficient to explain the whi2 phenotype since ectopic expression of CLN 1 in a nutrient‐depleted culture caused cells to continue dividing and interfered with the acquisition of heat resistance. These observations show that, either directly or indirectly, Whi2 negatively regulates G1 cyclin expression. Interestingly extremely high levels of Cln1 induced filamentous growth upon nutrient deprivation, suggesting a direct connection between G1 cyclin activity and morphological responses to poor nutrient conditions. © 1997 John Wiley & Sons, Ltd.