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

Abstract

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 β-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.).

Keywords: Cytoplasmic Ca2+; Flooding stress; H2S; Hypoxia tolerance; Maize; NO.