Dissemin is shutting down on January 1st, 2025

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Taylor and Francis Group, Autophagy, 4(9), p. 609-611

DOI: 10.4161/auto.23460

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Sulfide as a signaling molecule in autophagy

Journal article published in 2013 by Cecilia Gotor ORCID, Irene García, José L. Crespo, Luis C. Romero ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

Abstract

Hydrogen sulfide is already recognized as an important signaling molecule in mammalian systems, and emerging data suggest that H 2S is a signaling molecule just as important as nitric oxide (NO) and H 2O 2 in plants. Although sulfide is generated in chloroplasts and mitochondria, it is present predominantly in the charged HS (-) form due to the basic pH inside both organelles, thus requiring an active transporter, which is yet to be identified, to be released. In Arabidopsis, we found that the cytosolic L-cysteine desulfhydrase DES1 is involved in the degradation of cysteine, and therefore responsible for the generation of H 2S in this cellular compartment. DES1 deficiency leads to the induction of autophagy. Moreover, we have demonstrated that sulfide in particular exerts a general effect on autophagy through negative regulation, in a way unrelated to nutrient deficiency. The mechanisms of H 2S action and its molecular targets are largely unknown, although in animal systems, protein S-sulfhydration has been proposed as a mechanism for sulfide-mediated signaling.