数字农科院2.0

Atwakl10, a cell wall associated receptor-like kinase, negatively regulates leaf senescence in arabidopsis thaliana

文献类型： 外文期刊

作者： Li Lu;Li Kui;Ali Akhtar;Guo Yongfeng

作者机构：

关键词： Arabidopsis; AtWAKL10; Cell expansin; Cell wall associated receptor-like kinase; Defense responsive; Leaf senescence; WRKY transcription factors

期刊名称： International Journal of Molecular Sciences

ISSN： 1661-6596

年卷期： 2021 年 22 卷 9 期

页码：

收录情况： JCR（2021版）

摘要： Receptor-like kinases (RLKs) constitute a large group of cell surface receptors that play crucial roles in multiple biological processes. However, the function of most RLKs in plants has not been extensively explored, and much less for the class of cell wall associated kinases (WAKs) and WAK-like kinases (WAKLs). In this study, analyses of developmental expression patterns uncovered a putative role of AtWAKL10 in modulating leaf senescence, which was further investigated at physiological and molecular levels. The expression level of AtWAKL10 increased with the developmental progression and was rapidly upregulated in senescing leaf tissues. The promoter of AtWAKL10 contains various defense and hormone responsive elements, and its expression could be significantly induced by exogenous ABA, JA and SA. Moreover, the loss-of-function atwakl10 mutant showed earlier senescence along the course of natural development and accelerated leaf senescence under darkness and hormonal stresses, while plants overexpressing AtWAKL10 showed an opposite trend. Additionally, some defense and senescence related WRKY transcription factors could bind to the promoter of AtWAKL10. In addition, deletion and overexpression of AtWAKL10 caused several specific transcriptional alterations, including genes involved in cell extension, cell wall modification, defense response and senescence related WRKYs, which may be implicated in regulatory mechanisms adopted by AtWAKL10 in controlling leaf senescence. Taken together, these results revealed that AtWAKL10 negatively regulated leaf senescence. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

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