Hydrogen sulfide is required for salicylic acid-induced chilling tolerance of cucumber seedlings.

Abstract

Salicylic acid (SA) and hydrogen sulfide (H2S) have been proved to be multifunctional signal molecules to participate in the response of plants to abiotic stresses. However, it is still unclear whether there is interaction between SA and H2S in response to chilling intensity of cucumber seedlings. Here, we found SA was sensitive to chilling intensity. Under normal condition, NaHS (H2S donor) or removing endogenous H2S with hypotaurine (HT, a specific scavenger of H2S) and DL-propargylglycine (PAG, a specific inhibitor of H2S) has no effect on endogenous SA level; however, SA induced endogenous H2S content and activated the activities and mRNA level of L-/D-cysteine desulfhydrase (L-/D-CD), and inhibiting endogenous SA with paclobutrazol (PAC) or 2-aminoindan-2-phosphonic acid (AIP) blocked this effect, implying H2S may play a role after SA signal. Further studies showed that both SA and NaHS notably alleviated chilling injury, which was evidenced by lower electrolyte leakage (EL), MDA content, and ROS accumulation, compared with H2O treatment. Of note, SA and H2S improved the activities and mRNA level of antioxidant enzymes (SOD, POD, CAT, APX, and GR) as well as the contents of AsA and GSH. Additionally, the chilling-response genes (ICE, CBF1, and COR) were obviously upregulated by exogenous SA and NaHS. However, the positive effect of SA on chilling tolerance was inhibited by HT, whereas PAC or AIP did not affect NaHS-induced chilling tolerance. Taken together, the data reveals that H2S acts as a downstream signal of SA-induced chilling tolerance of cucumber via modulating antioxidant system and chilling-response genes.