Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/25309

TitleInvolvement of yeast HSP90 isoforms in response to stress and cell death induced by acetic acid
Author(s)Silva, Maria Alexandra
Marques, Belém Sampaio
Fernandes, Ângela Margarida Oliveira
Carreto, Laura
Rodrigues, Fernando José dos Santos
Holcik, Martin
Santos, Manuel A. S.
Ludovico, Paula
Issue date2013
PublisherPLOS
JournalPLoS ONE
Abstract(s)Acetic acid-induced apoptosis in yeast is accompanied by an impairment of the general protein synthesis machinery, yet paradoxically also by the up-regulation of the two isoforms of the heat shock protein 90 (HSP90) chaperone family, Hsc82p and Hsp82p. Herein, we show that impairment of cap-dependent translation initiation induced by acetic acid is caused by the phosphorylation and inactivation of eIF2 alpha by Gcn2p kinase. A microarray analysis of polysome-associated mRNAs engaged in translation in acetic acid challenged cells further revealed that HSP90 mRNAs are over-represented in this polysome fraction suggesting preferential translation of HSP90 upon acetic acid treatment. The relevance of HSP90 isoform translation during programmed cell death (PCD) was unveiled using genetic and pharmacological abrogation of HSP90, which suggests opposing roles for HSP90 isoforms in cell survival and death. Hsc82p appears to promote survival and its deletion leads to necrotic cell death, while Hsp82p is a pro-death molecule involved in acetic acid-induced apoptosis. Therefore, HSP90 isoforms have distinct roles in the control of cell fate during PCD and their selective translation regulates cellular response to acetic acid stress.
TypeArticle
URIhttp://hdl.handle.net/1822/25309
DOI10.1371/journal.pone.0071294
ISSN1932-6203
Publisher versionhttp://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0071294
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

Files in This Item:
File Description SizeFormat 
silva a_plosone 2013.pdf1,22 MBAdobe PDFView/Open

Partilhe no FacebookPartilhe no TwitterPartilhe no DeliciousPartilhe no LinkedInPartilhe no DiggAdicionar ao Google BookmarksPartilhe no MySpacePartilhe no Orkut
Exporte no formato BibTex mendeley Exporte no formato Endnote Adicione ao seu ORCID