- THIS ARTICLE
- Full Text
- Full Text (PDF)
-
All Versions of this Article:
genetics.106.059873v1
174/3/1135 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- 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 Ruault, M.
- Articles by Pillus, L.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Ruault, M.
- Articles by Pillus, L.
Originally published as Genetics Published Articles Ahead of Print on September 1, 2006.
Genetics, Vol. 174, 1135-1149, November 2006, Copyright © 2006
doi:10.1534/genetics.106.059873
Chromatin-Modifiying Enzymes Are Essential When the Saccharomyces cerevisiae Morphogenesis Checkpoint Is Constitutively Activated
Myriam Ruault and Lorraine Pillus1
Division of Biological Sciences, UCSD Moores Cancer Center and Center for Molecular Genetics, University of California, San Diego, California 92093-0347.
1 Corresponding author: 9500 Gilman Dr., University of California, La Jolla, CA 92093-0347.
E-mail: lpillus{at}ucsd.edu
Hsl7p plays a central role in the morphogenesis checkpoint triggered when yeast bud formation is impaired and is proposed to function as an arginine methyltransferase. HSL7 is also essential in the absence of the N-terminal tails of histones H3 or H4. The requirement for H3 and H4 tails may indicate a need for their post-translational modification to bypass the morphogenesis checkpoint. In support of this, the absence of the acetyltransferases Gcn5p or Esa1p, the deacetylase Rpd3p, or the lysine-methyltransferase Set1p resulted in death or extreme sickness in hsl
mutants. These synthetic interactions involved both the activity of the chromatin-modifying enzymes and the complexes through which they act. Newly reported silencing phenotypes of hsl7 mirror those previously reported for gcn5 and rpd3, thereby strengthening their functional links. In addition, synthetic interactions and silencing phenotypes were suppressed by inactivation of the morphogenesis checkpoint, either by SWE1 deletion or by preventing Cdc28p phosphorylation. A catalytically dead Hsl7p retained wild-type interactions, implying that modification of histone H3 or H4 N termini by Gcn5p, Esa1p, Rpd3p, and Set1p, but not by Hsl7p, was needed to bypass the morphogenesis checkpoint.
This article has been cited by other articles:
 |
|
 |
|
  E. B. Gomez, R. L. Nugent, S. Laria, and S. L. Forsburg Schizosaccharomyces pombe Histone Acetyltransferase Mst1 (KAT5) Is an Essential Protein Required for Damage Response and Chromosome Segregation Genetics, June 1, 2008; 179(2): 757 - 771. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Bachand Protein Arginine Methyltransferases: from Unicellular Eukaryotes to Humans Eukaryot. Cell, June 1, 2007; 6(6): 889 - 898. [Full Text] [PDF]
|
|