AtWAKL10, a Cell Wall Associated Receptor-Like Kinase, Negatively Regulates Leaf Senescence in Arabidopsis thaliana.

AtWAKL10, a Cell Wall Associated Receptor-Like Kinase, Negatively Regulates Leaf Senescence in Arabidopsis thaliana.
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细胞壁相关受体样激酶AtWAKL10负向调控拟南芥叶片衰老。

DOI:
10.3390/ijms22094885
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发表时间:
2021-05-05
影响因子:
5.6
通讯作者:
Guo Y
Guo Y
中科院分区:
生物学2区
文献类型:
--
作者:
Li L;Li K;Ali A;Guo Y

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受体样激酶(RLK)构成一大类细胞表面受体,在多种生物过程中发挥着至关重要的作用。然而,大多数 RLK 在植物中的功能尚未得到广泛探索,更不用说细胞壁相关激酶 (WAK) 和 WAK 样激酶 (WAKL) 类别了。在这项研究中,对发育表达模式的分析揭示了 AtWAKL10 在调节叶片衰老中的假定作用,并在生理和分子水平上进行了进一步研究。 AtWAKL10的表达水平随着发育进程而增加,并且在衰老的叶组织中迅速上调。 AtWAKL10的启动子含有多种防御和激素反应元件,其表达可被外源ABA、JA和SA显着诱导。此外,功能缺失的atwakl10突变体在自然发育过程中表现出较早的衰老,并在黑暗和激素胁迫下加速叶片衰老,而过表达AtWAKL10的植物则表现出相反的趋势。此外,一些防御和衰老相关的 WRKY 转录因子可以与 AtWAKL10 的启动子结合。此外,AtWAKL10的缺失和过表达引起了一些特定的转录改变,包括涉及细胞延伸、细胞壁修饰、防御反应和衰老相关WRKY的基因,这些基因可能与AtWAKL10控制叶片衰老的调节机制有关。综上所述,这些结果表明 AtWAKL10 负向调节叶片衰老。
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.
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