Functional analysis of the role of hydrogen sulfide in the regulation of dark-induced leaf senescence in Arabidopsis

Abstract There is growing evidence that hydrogen sulfide (H2S) is involved in many physiological processes in plants, but the role of H2S in dark-induced leaf senescence remains unknown. In this work, we found that H2S not only inhibited chlorophyll degradation but also caused the accumulation of ph...

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Autores principales: Bo Wei, Wei Zhang, Jin Chao, Tianru Zhang, Tingting Zhao, Graham Noctor, Yongsheng Liu, Yi Han
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/dd81e1a7903942cdab0fd3aa9f8de124
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Sumario:Abstract There is growing evidence that hydrogen sulfide (H2S) is involved in many physiological processes in plants, but the role of H2S in dark-induced leaf senescence remains unknown. In this work, we found that H2S not only inhibited chlorophyll degradation but also caused the accumulation of photoreactive pheide a in detached leaves under extended darkness. Despite this, transcript levels of senescence-associated genes (SAGs) were less affected in H2S-treated detached leaves compared with those in H2S-untreated detached leaves. Furthermore, cell death/rapid bleaching occurred in both H2S-treated detached and attached leaves after transfer from extended darkness to light. Unlike the lack of effect of H2S on SAG transcripts in darkened detached leaves, exogenous H2S induced higher SAG transcript levels in attached leaves than untreated attached leaves. Genetic evidence further underlined the positive correlation between SAG expression in attached leaves and H2S. In addition, effects of H2S on SAG expression in attached leaves were compromised in the S-nitrosoglutathione reductase-deficient mutant, gsnor1. Taken together, our results suggest that H2S suppresses chlorophyll degradation of detached leaves by regulating a dark-dependent reaction, and that this gas positively modulates SAG expression in attached leaves under prolonged darkness in a GSNOR1-dependent manner.