Yeast caspase 1 links messenger RNA stability to apoptosis in yeast

During the past years, yeasts have been successfully established as models to study the mechanisms of apoptotic regulation. We recently showed that mutations in the LSM4 gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mi...

Full description

Saved in:
Bibliographic Details
Published inEMBO reports Vol. 6; no. 11; pp. 1076 - 1081
Main Authors Mazzoni, Cristina, Herker, Eva, Palermo, Vanessa, Jungwirth, Helmut, Eisenberg, Tobias, Madeo, Frank, Falcone, Claudio
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.11.2005
Blackwell Publishing Ltd
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:During the past years, yeasts have been successfully established as models to study the mechanisms of apoptotic regulation. We recently showed that mutations in the LSM4 gene, which is involved in messenger RNA decapping, lead to increased mRNA stability and apoptosis in yeast. Here, we show that mitochondrial function and YCA1, which encodes a budding yeast metacaspase, are necessary for apoptosis triggered by stabilization of mRNAs. Deletion of YCA1 in yeast cells mutated in the LSM4 gene prevents mitochondrial fragmentation and rapid cell death during chronological ageing of the culture, diminishes reactive oxygen species accumulation and DNA breakage, and increases resistance to H2O2 and acetic acid. mRNA levels in lsm4 mutants deleted for YCA1 are still increased, positioning the Yca1 budding yeast caspase as a downstream executor of cell death induced by mRNA perturbations. In addition, we show that mitochondrial function is necessary for fast death during chronological ageing, as well as in LSM4 mutated and wild‐type cells.
Bibliography:ark:/67375/WNG-LSCHWBGS-4
istex:09DA316B849A5BCEAD71D41CF0BD005871DE4C28
ArticleID:EMBR7400514
Supplementary Figure 1
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1469-221X
1469-3178
1469-221X
DOI:10.1038/sj.embor.7400514