Is oxidized thioredoxin a major trigger for cysteine oxidation? Clues from a redox proteomics approach
Article, Other literature type
García Santamarina, Sarela, 1978-
Boronat i Llop, Susanna, 1965-
Calvo, Isabel A.
Rodríguez Gabriel, Miguel
Ayté del Olmo, José
Hidalgo Hernando, Elena
- Publisher: Mary Ann Liebert, Inc
Reacció d'oxidació-reducció | Thioredoxin | Cysteine | Oxidation | Glicoproteïnes | News & Views | Cytoplasmic thiol homeostasis | Biología y Biomedicina / Biología
mesheuropmc: animal structures
This is a copy of an article published in the Antioxidants & Redox Signaling © Mary Ann Liebert, Inc. Antioxidants & Redox Signaling is available online at http://online.liebertpub.com
Cysteine oxidation mediates oxidative stress toxicity and signaling. It has been long proposed that the thioredoxin
(Trx) system, which consists of Trx and thioredoxin reductase (Trr), is not only involved in recycling
classical Trx substrates, such as ribonucleotide reductase, but it also regulates general cytoplasmic thiol homeostasis.
To investigate such a role, we have performed a proteome-wide analysis of cells expressing or not the
two components of the Trx system. We have compared the reversibly oxidized thiol proteomes of wild-type
Schizosaccharomyces pombe cells with mutants lacking Trx or Trr. Specific Trx substrates are reversibly-oxidized in
both strain backgrounds; however, in the absence of Trr, Trx can weakly recycle its substrates at the expense of
an alternative electron donor. A massive thiol oxidation occurs only in cells lacking Trr, with 30% of all cysteinecontaining
peptides being reversibly oxidized; this oxidized cysteine proteome depends on the presence of Trxs.
Our observations lead to the hypothesis that, in the absence of its reductase, the natural electron donor Trx
becomes a powerful oxidant and triggers general thiol oxidation.
This work was supported by the Spanish Ministry of Science
and Innovation (BFU2009-06933 and BFU2012-32045),
PLAN E and FEDER, by the Spanish program Consolider-
Ingenio 2010 Grant CSD 2007-0020, and by SGR2009-196 from
Generalitat de Catalunya (Spain) to E.H. E. H. and J.A. are
recipients of ICREA Academia Awards (Generalitat de