Arabidopsis thaliana CRK41 negatively regulates salt tolerance via H2O2 and ABA cross-linked networks

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.