Journal
CELL METABOLISM
Volume 30, Issue 6, Pages 1152-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2019.10.007
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Funding
- ATIP-Avenir grant
- French State [ANR-10-IDEX-03-02]
- FRM [DEQ20180339181]
- MRC, UK [MR/M022706/1]
- Brian Ridge Scholarship
- Northcott Devon Medical Research Foundation, UK
- Ministry of Education, Science and Technology Development of the Republic of Serbia [173009]
- NIH [GM102187]
- DFG, Germany [SFB1218 TP B08]
- AHA/Allen Initiative in Brain Health and Cognitive Impairment team (SHS and associates) [19PABH134580006]
- MRC [MR/S002626/1, MC_PC_16044] Funding Source: UKRI
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Life on Earth emerged in a hydrogen sulfide (H2S)-rich environment eons ago and with it protein persulfidation mediated by H2S evolved as a signaling mechanism. Protein persulfidation (S-sulfhydration) is a post-translational modification of reactive cysteine residues, which modulate protein structure and/or function. Persulfides are difficult to label and study due to their reactivity and similarity with cysteine. Here, we report a facile strategy for chemoselective persulfide bioconjugation using dimedone-based probes, to achieve highly selective, rapid, and robust persulfide labeling in biological samples with broad utility. Using this method, we show persulfidation is an evolutionarily conserved modification and waves of persulfidation are employed by cells to resolve sulfenylation and prevent irreversible cysteine overoxidation preserving protein function. We report an age-associated decline in persulfidation that is conserved across evolutionary boundaries. Accordingly, dietary or pharmacological interventions to increase persulfidation associate with increased longevity and improved capacity to cope with stress stimuli.
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