- THIS ARTICLE
- Full Text
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Email this article to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Manukyan, A.
- Articles by Schneider, B. L.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Manukyan, A.
- Articles by Schneider, B. L.
Genetics, Vol. 179, 345-357, May 2008, Copyright © 2008
doi:10.1534/genetics.108.086744
Ccr4 Alters Cell Size in Yeast by Modulating the Timing of CLN1 and CLN2 Expression
Arkadi Manukyan, Jian Zhang1, Uma Thippeswamy, Jingye Yang, Noelle Zavala, Malkanthi P. Mudannayake, Mark Asmussen, Colette Schneider and Brandt L. Schneider2
Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, Texas 79430
2 Corresponding author: Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430.
E-mail: brandt.schneider{at}ttuhsc.edu
Large, multisubunit Ccr4-Not complexes are evolutionarily conserved global regulators of gene expression. Deletion of CCR4 or several components of Ccr4-Not complexes results in abnormally large cells. Since yeast must attain a critical cell size at Start to commit to division, the large size of ccr4
cells implies that they may have a size-specific proliferation defect. Overexpression of CLN1, CLN2, CLN3, and SWI4 reduces the size of ccr4 cells, suggesting that ccr4 cells have a G1-phase cyclin deficiency. In support of this, we find that CLN1 and CLN2 expression and budding are delayed in ccr4 cells. Moreover, overexpression of CCR4 advances the timing of CLN1 expression, promotes premature budding, and reduces cell size. Genetic analyses suggest that Ccr4 functions independently of Cln3 and downstream of Bck2. Thus, like cln3bck2 double deletions, cln3ccr4 cells are also inviable. However, deletion of Whi5, a transcriptional repressor of CLN1 and CLN2, restores viability. We find that Ccr4 negatively regulates the half-life of WHI5 mRNAs, and we conclude that, by modulating the stability of WHI5 mRNAs, Ccr4 influences the size-dependent timing of G1-phase cyclin transcription.
This article has been cited by other articles:
 |
|
 |
|
  A. Traven, T. H. Beilharz, T. L. Lo, F. Lueder, T. Preiss, and J. Heierhorst The Ccr4-Pop2-NOT mRNA Deadenylase Contributes to Septin Organization in Saccharomyces cerevisiae Genetics, August 1, 2009; 182(4): 955 - 966. [Abstract] [Full Text] [PDF]
|
|
|