Cloning and expression profiling of the PacSnRK2 and PacPP2C gene families during fruit development, ABA treatment, and dehydration stress in sweet cherry

文献类型： 外文期刊

第一作者： Shen, Xinjie

作者： Shen, Xinjie;Zhao, Wei;Shen, Xinjie;Guo, Xiao;Zhao, Di;Wang, Yantao;Peng, Xiang;Wei, Yan;Zhai, Zefeng;Li, Tianhong;Zhang, Qiang;Jiang, Yuzhuang;Li, Tianhong

作者机构：

关键词： ABA;Dehydration stress;PP2C;Prunus avium;Sweet cherry fruit;SnRK2

期刊名称：PLANT PHYSIOLOGY AND BIOCHEMISTRY （ 影响因子：4.27； 五年影响因子：4.816 ）

ISSN： 0981-9428

年卷期： 2017 年 119 卷

页码：

收录情况： SCI

摘要： Plant SNF1-related protein kinase 2 (SnRK2) and protein phosphatase 2C (PP2C) family members are core components of the ABA signal transduction pathway. SnRK2 and PP2C proteins have been suggested to play crucial roles in fruit ripening and improving plant tolerance to drought stress, but supporting genetic information has been lacking in sweet cherry (Prunus avium L.). Here, we cloned six full-length SnRK2 genes and three full-length PP2C genes from sweet cherry cv. Hong Deng. Quantitative PCR analysis revealed that PacSnRK2.2, PacSnRK2.3, PacSnRK2.6, and PacPP2C1-3 were negatively regulated in fruits in response to exogenous ABA treatment, PacSnRK2.4 and PacSnRK2.5 were upregulated, and PacSnRK2.1 expression was not affected. The ABA treatment also significantly promoted the accumulation of anthocyanins in sweet cherry fruit. The expression of all PacSnRK2 and PacPP2C genes was induced by dehydration stress, which also promoted the accumulation of drought stress signaling molecules in the sweet cherry fruits, including ABA, soluble sugars, and anthocyanin. Furthermore, a yeast two-hybrid analysis demonstrated that PacPP2C1 interacts with all six PacSnRK2s, while PacPP2C3 does not interact with PacSnRK2.5. PacPP2C2 does not interact with PacSnRK2.1 or PacSnRK2.4. These results indicate that PacSnRK2s and PacPP2Cs may play a variety of roles in the sweet cherry ABA signaling pathway and the fruit response to drought stress. (C) 2017 Elsevier Masson SAS. All rights reserved.

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