Copper exposure effects on yeast mitochondrial proteome

Mitochondria play an important role on the entire cellular copper homeostatic mechanisms. Alteration of cellular copper levels may thus influence mitochondrial proteome and its investigation represents an important contribution to the general understanding of copper-related cellular effects. In thes...

Full description

Saved in:
Bibliographic Details
Published inJournal of proteomics Vol. 74; no. 11; pp. 2522 - 2535
Main Authors Banci, Lucia, Bertini, Ivano, Ciofi-Baffoni, Simone, D'Alessandro, Annamaria, Jaiswal, Deepa, Marzano, Valeria, Neri, Sara, Ronci, Maurizio, Urbani, Andrea
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 19.10.2011
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Mitochondria play an important role on the entire cellular copper homeostatic mechanisms. Alteration of cellular copper levels may thus influence mitochondrial proteome and its investigation represents an important contribution to the general understanding of copper-related cellular effects. In these study we have performed an organelle targeted proteomic investigation focusing our attention on the effect of non-lethal 1 mM copper concentration on Saccharomyces cerevisiae mitochondrial proteome. Functional copper effects on yeast mitochondrial proteome were evaluated by using both 2D electrophoresis (2-DE) and liquid chromatography coupled with tandem mass spectrometry. Proteomic data have been then analyzed by different unsupervised meta-analysis approaches that highlight the impairment of mitochondrial functions and the activation of oxidative stress response. Interestingly, our data have shown that stress response generated by 1 mM copper treatment determines the activation of S. cerevisiae survival pathway. To investigate these findings we have treated yeast cells responsiveness to copper with hydrogen peroxide and observed a protective role of this metal. These results are suggestive of a copper role in the protection from oxidative stress possibly due to the activation of mechanisms involved in cellular survival and growth. [Display omitted]
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:1874-3919
1876-7737
DOI:10.1016/j.jprot.2011.04.014