Hydrogen sulfide enhances nitric oxide-induced tolerance of hypoxia in maize (Zea mays L.)

Our data present H (2) S in a new role, serving as a multi-faceted transducer to different response mechanisms during NO-induced acquisition of tolerance to flooding-induced hypoxia in maize seedling roots. Nitric oxide (NO), serving as a secondary messenger, modulates physiological processes in plants. Recently, hydrogen sulfide (H2S) has been demonstrated to have similar signaling functions. This study focused on the effects of treatment with H2S on NO-induced hypoxia tolerance in maize seedlings. The results showed that treatment with the NO donor sodium nitroprusside (SNP) enhanced survival rate of submerged maize roots through induced accumulation of endogenous H2S. The induced H2S then enhanced endogenous Ca2+ levels as well as the Ca2+-dependent activity of alcohol dehydrogenase (ADH), improving the capacity for antioxidant defense and, ultimately, the hypoxia tolerance in maize seedlings. In addition, NO induced the activities of key enzymes in H2S biosynthesis, such as l-cysteine desulfhydrases (l-CDs), O-acetyl-l-serine (thiol)lyase (OAS-TL), and beta-Cyanoalanine Synthase (CAS). SNP-induced hypoxia tolerance was enhanced by the application of NaHS, but was eliminated by the H2S-synthesis inhibitor hydroxylamine (HA) and the H2S-scavenger hypotaurine (HT). H2S concurrently enhanced the transcriptional levels of relative hypoxia-induced genes. Together, our findings indicated that H2S serves as a multi-faceted transducer that enhances the nitric oxide-induced hypoxia tolerance in maize (Zea mays L.).