Abstract Cysteine-rich receptor-like kinases (CRKs) play important roles in multiple stress responses. However, little was known about CRKs-mediated salt stress tolerance in plants. In this study, we identified a plasma membrane localized CRK41, which was mainly expressed in leaves and rapidly response to NaCl and abscisic acid (ABA) treatments. Though the growth phenotype was not influenced by changing CRK41 transcripts via genetic approach, we found that CRK41 negatively regulated salt tolerance through survival rates analysis. Furthermore, RbohD-induced hydrogen peroxide (H2O2) played essential role in activating the CRK41 transcript under salt stress. Meanwhile, up-regulation of CRK41 further induced H2O2 accumulation by inhibiting three main antioxidant enzymes (SOD, APX, and CAT), which resulted lipid peroxidation and cell death. Importantly, high transcript of CRK41 reduced the ABA concentration and signaling sensibility by analyzing several ABA-induced typical phenotypes and ABA-related genes’ expression. These results were also supported by the genes expression patterns of wild-type (WT) and crk41 mutant in NaCl and ABA treatments by interactive transcriptome analysis. Additionally, we found that CRK41-mediated both H2O2 and ABA signaling took part in NaCl-induced cell death by activating MAPK3 and MAPK6 under salt condition. Taken together, the present study suggests that CRK41 negatively regulated Arabidopsis thaliana salt tolerance by magnifying H2O2 signaling and inhibiting ABA signaling, which mainly cross-linked with MAPK signaling to control salt-induced cell death.

中文翻译：

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拟南芥 CRK41 通过 H2O2 和 ABA 交联网络负调节耐盐性

摘要 富含半胱氨酸的受体样激酶 (CRKs) 在多种应激反应中发挥重要作用。然而，人们对 CRKs 介导的植物盐胁迫耐受性知之甚少。在这项研究中，我们鉴定了一种质膜定位的 CRK41，它主要在叶片中表达，并且对 NaCl 和脱落酸 (ABA) 处理具有快速反应。虽然生长表型不受通过遗传方法改变 CRK41 转录本的影响，但我们发现 CRK41 通过存活率分析负调节耐盐性。此外，RbohD 诱导的过氧化氢 (H2O2) 在盐胁迫下激活 CRK41 转录物方面发挥了重要作用。同时，CRK41 的上调通过抑制三种主要抗氧化酶（SOD、APX 和 CAT）进一步诱导 H2O2 积累，从而导致脂质过氧化和细胞死亡。重要的，通过分析几种 ABA 诱导的典型表型和 ABA 相关基因的表达，CRK41 的高转录本降低了 ABA 浓度和信号敏感性。通过交互式转录组分析，这些结果也得到了 NaCl 和 ABA 处理中野生型 (WT) 和 crk41 突变体的基因表达模式的支持。此外，我们发现 CRK41 介导的 H2O2 和 ABA 信号通过在盐条件下激活 MAPK3 和 MAPK6 参与 NaCl 诱导的细胞死亡。综上所述，本研究表明 CRK41 通过放大 H2O2 信号和抑制 ABA 信号负向调节拟南芥的耐盐性，ABA 信号主要与 MAPK 信号交联以控制盐诱导的细胞死亡。