CmPYL7 positively regulates the cold tolerance via interacting with CmPP2C24-like in oriental melon.

Pyrabactin or Actin Resistance1/PYR1-Like/Regulatory Components of abscisic acid (ABA) Receptors (PYR/PYL/RCARs, referred to as PYLs) are direct receptors of ABA that function pivotally in the ABA-signaling pathway. Previously, we discovered that CmPYL7 was strongly upregulated by cold stress in oriental melon (Cucumis melo). In this study, we demonstrated that CmPYL7 was strongly induced by cold treatment (Cold), Cold+ABA, and Cold+fluridone (Flu, an ABA inhibitor) treatments, while the expression level of CmPYL7 under Cold+Flu is lower than that of cold treatment. Silencing CmPYL7 in oriental melon seedlings significantly decreased cold tolerance due to the reduced activities of antioxidant enzymes [superoxide dismutase (SOD); catalase (CAT), and ascorbate peroxidase (APX)] and the accumulation of HO, accompanied by higher electrolyte leakage and MDA content, but lower proline and soluble sugar content. In contrast, overexpressing CmPYL7 in Arabidopsis plants significantly increased cold tolerance owing to the enhanced activities of antioxidant enzymes (SOD, CAT, and APX) and limited HO, accompanied by lower electrolyte leakage and MDA content, but higher proline and soluble sugar contents. CmPYL7 was found to interact with CmPP2C24-like in vivo and in vitro, whose expression is downregulated under cold stress. Furthermore, silenced CmPP2C24-like in oriental melon plants significantly increased cold tolerance, exhibiting lower electrolyte leakage and MDA content and higher proline and soluble sugar contents. The activities of SOD, CAT, and APX were further enhanced and contents of HO were significantly limited from increasing in TRV-CmPP2C24-like seedlings. These results demonstrated that CmPYL7 functions positively in the ABA-signaling pathway to regulate cold tolerance by interacting with CmPP2C24-like protein.