Abstract
Hydrogen sulfide (H(2)S) plays a crucial role in regulating chilling tolerance. However, the role of hydrogen peroxide (H(2)O(2)) and auxin in H(2)S-induced signal transduction in the chilling stress response of plants was unclear. In this study, 1.0 mM exogenous H(2)O(2) and 75 μM indole-3-acetic acid (IAA) significantly improved the chilling tolerance of cucumber seedlings, as demonstrated by the mild plant chilling injury symptoms, lower chilling injury index (CI), electrolyte leakage (EL), and malondialdehyde content (MDA) as well as higher levels of photosynthesis and cold-responsive genes under chilling stress. IAA-induced chilling tolerance was weakened by N, N'-dimethylthiourea (DMTU, a scavenger of H(2)O(2)), but the polar transport inhibitor of IAA (1-naphthylphthalamic acid, NPA) did not affect H(2)O(2)-induced mitigation of chilling stress. IAA significantly enhanced endogenous H(2)O(2) synthesis, but H(2)O(2) had minimal effects on endogenous IAA content in cucumber seedlings. In addition, the H(2)O(2) scavenger DMTU, inhibitor of H(2)O(2) synthesis (diphenyleneiodonium chloride, DPI), and IAA polar transport inhibitor NPA reduced H(2)S-induced chilling tolerance. Sodium hydrosulfide (NaHS) increased H(2)O(2) and IAA levels, flavin monooxygenase (FMO) activity, and respiratory burst oxidase homolog (RBOH1) and FMO-like protein (YUCCA2) mRNA levels in cucumber seedlings. DMTU, DPI, and NPA diminished NaHS-induced H(2)O(2) production, but DMTU and DPI did not affect IAA levels induced by NaHS during chilling stress. Taken together, the present data indicate that H(2)O(2) as a downstream signal of IAA mediates H(2)S-induced chilling tolerance in cucumber seedlings.