State Key Laboratory of Crop Biology; Key Laboratory of Crop Biology and Genetic Improvement of Horticultural Crops in Huang huai Region; College of Horticulture Science and Engineering, Shandong Agricultural University, Tai'an, 271018, Shandong, China.
Protoplasma. 2020 Nov;257(6):1543-1557. doi: 10.1007/s00709-020-01531-y. Epub 2020 Jul 3.
Salicylic acid (SA) and hydrogen sulfide (HS) 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 HS in response to chilling intensity of cucumber seedlings. Here, we found SA was sensitive to chilling intensity. Under normal condition, NaHS (HS donor) or removing endogenous HS with hypotaurine (HT, a specific scavenger of HS) and DL-propargylglycine (PAG, a specific inhibitor of HS) has no effect on endogenous SA level; however, SA induced endogenous HS 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 HS 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 HO treatment. Of note, SA and HS 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 HS acts as a downstream signal of SA-induced chilling tolerance of cucumber via modulating antioxidant system and chilling-response genes.
水杨酸（SA）和硫化氢（HS）已被证明是多功能信号分子，参与植物对非生物胁迫的响应。然而，SA 和 HS 是否在黄瓜幼苗对低温胁迫的响应中存在相互作用尚不清楚。在这里，我们发现 SA 对低温胁迫敏感。在正常条件下，NaHS（HS 供体）或用高半胱氨酸（HT，HS 的特异性清除剂）和 DL-炔丙基甘氨酸（PAG，HS 的特异性抑制剂）去除内源性 HS 对内源 SA 水平没有影响；然而，SA 诱导内源性 HS 含量并激活 L-/D-半胱氨酸脱硫酶（L-/D-CD）的活性和 mRNA 水平，并用多效唑（PAC）或 2-氨基茚满-2-膦酸（AIP）抑制内源 SA 则阻断了这一效应，表明 HS 可能在 SA 信号之后发挥作用。进一步的研究表明，SA 和 NaHS 都明显减轻了低温伤害，与 HO 处理相比，电导率（EL）、MDA 含量和 ROS 积累较低。值得注意的是，SA 和 HS 提高了抗氧化酶（SOD、POD、CAT、APX 和 GR）的活性和 mRNA 水平以及 AsA 和 GSH 的含量。此外，外源 SA 和 NaHS 明显上调了低温响应基因（ICE、CBF1 和 COR）。然而，HT 抑制了 SA 对低温胁迫耐性的正向作用，而 PAC 或 AIP 并不影响 NaHS 诱导的低温胁迫耐性。总之，这些数据表明 HS 通过调节抗氧化系统和低温响应基因作为 SA 诱导黄瓜低温耐性的下游信号。
