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Vol. 17, Issue 3, 1164-1175, March 2006

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Sphingoid Base Is Required for Translation Initiation during Heat Stress in Saccharomyces cerevisiae

Karsten D. Meier ^*, Olivier Deloche , Kentaro Kajiwara , Kouichi Funato , and Howard Riezman 

Department of Biochemistry, University of Geneva, CH-1211 Geneva 4, Switzerland; ^* Department of Biochemistry, Biozentrum of the University of Basel, CH-4056 Basel, Switzerland; Department of Microbiology and Molecular Medicine, CMU, University of Geneva, CH-1211 Geneva 4, Switzerland; and Graduate School of Biosphere Science, Faculty of Applied Biological Science, Hiroshima University, Higashi-Hiroshima 739-8528, Japan

Submitted November 14, 2005; Revised December 13, 2005; Accepted December 20, 2005
Monitoring Editor: Sean Munro

Sphingolipids are required for many cellular functions including response to heat shock. We analyzed the yeast lcb1-100 mutant, which is conditionally impaired in the first step of sphingolipid biosynthesis and shows a strong decrease in heat shock protein synthesis and viability. Transcription and nuclear export of heat shock protein mRNAs is not affected. However, lcb1-100 cells exhibited a strong decrease in protein synthesis caused by a defect in translation initiation under heat stress conditions. The essential lipid is sphingoid base, not ceramide or sphingoid base phosphates. Deletion of the eIF4E-binding protein Eap1p in lcb-100 cells restored translation of heat shock proteins and increased viability. The translation defect during heat stress in lcb1-100 was due at least partially to a reduced function of the sphingoid base-activated PKH1/2 protein kinases. In addition, depletion of the translation initiation factor eIF4G was observed in lcb1-100 cells and ubiquitin overexpression allowed partial recovery of translation after heat stress. Taken together, we have shown a requirement for sphingoid bases during the recovery from heat shock and suggest that this reflects a direct lipid-dependent signal to the cap-dependent translation initiation apparatus.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

Address correspondence to: Howard Riezman (howard.riezman{at}biochem.unige.ch).

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