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桃叶芽的内休眠解除可由GA-GID1c-DELLA2模块调控。

Endodormancy Release Can Be Modulated by the GA-GID1c-DELLA2 Module in Peach Leaf Buds.

作者信息

Li Sen, Wang Qingjie, Wen Binbin, Zhang Rui, Jing Xiuli, Xiao Wei, Chen Xiude, Tan Qiuping, Li Ling

机构信息

College of Horticulture Science and Engineering, Shandong Agricultural University, Tai'an, China.

State Key Laboratory of Crop Biology, Shandong Agricultural University, Tai'an, China.

出版信息

Front Plant Sci. 2021 Sep 27;12:713514. doi: 10.3389/fpls.2021.713514. eCollection 2021.

Abstract

Gibberellin (GA) plays a key role in the release of bud dormancy and the GA receptor GID1 (GIBBERELLIN INSENSITIVE DWARF1) and DELLA protein are the GA signaling parts, but the molecular mechanism of GA-GID1-DELLA module regulating leaf bud dormancy in peach () is still not very clear. In this study, we isolated and characterized the GID1 gene from the peach cultivar "Zhong you No.4." Overexpressing in promoted seed germination, which indicated that has an important function in dormancy. The expression level of PpGID1c in peach leaf buds during endodormancy release was higher than that during ecodormancy and was positively correlated with GA levels. Our study also found that GA had the most obvious effect on promoting the bud break, indicating that GA may be the key gibberellin to promoting peach leaf bud endodormancy release. Moreover, a quantitative real-time PCR (qRT-PCR) found that GA could increase the expression of the gibberellin signaling gene . A yeast two-hybrid (Y2H) assay suggested that the PpGID1c interaction with the PpDELLA1 protein was not dependent on gibberellin, while the PpGID1c interaction with PpDELLA2 required GA or another gibberellin. These findings suggested that the GA-GID1c-DELLA2 module regulates peach leaf bud endodormancy release, with this finding significantly enhancing our comprehensive understanding of bud endodormancy release and revealing a new mechanism for regulating leaf bud endodormancy release in peach.

摘要

赤霉素(GA)在打破芽休眠过程中起关键作用,GA受体GID1(赤霉素不敏感矮化蛋白1)和DELLA蛋白是GA信号传导元件,但GA-GID1-DELLA模块调控桃()叶芽休眠的分子机制仍不是很清楚。在本研究中,我们从桃品种“中油4号”中分离并鉴定了GID1基因。在中过表达促进了种子萌发,这表明在休眠中具有重要功能。在深休眠解除过程中,桃叶芽中PpGID1c的表达水平高于生态休眠期间,且与GA水平呈正相关。我们的研究还发现,GA对促进芽萌发的作用最明显,这表明GA可能是促进桃叶芽深休眠解除的关键赤霉素。此外,定量实时PCR(qRT-PCR)发现,GA可增加赤霉素信号基因的表达。酵母双杂交(Y2H)试验表明,PpGID1c与PpDELLA1蛋白的相互作用不依赖于赤霉素,而PpGID1c与PpDELLA2的相互作用需要GA或另一种赤霉素。这些发现表明,GA-GID1c-DELLA2模块调控桃叶芽深休眠的解除,这一发现显著增强了我们对芽深休眠解除的全面理解,并揭示了调控桃叶芽深休眠解除的新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/723b/8504481/270518fea584/fpls-12-713514-g0001.jpg

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