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Plant Cell:泛素连接酶ATL31和ATL6通过介导CPK28的泛素化和降解,精细调控拟南芥的免疫

已有 881 次阅读 2021-10-3 09:30 |个人分类:每日摘要|系统分类:论文交流

The calcium-dependent protein kinase CPK28 is targeted by the ubiquitin ligases ATL31 and ATL6 for proteasome-mediated degradation to fine-tune immune signaling in Arabidopsis

第一作者Xiaotong Liu

第一单位中科院遗传与发育生物学研究所

第一通讯Dongping Lu


 Abstract 


背景回顾Immune responses are triggered when pattern recognition receptors (PRRs) recognize microbial molecular patterns. The Arabidopsis (Arabidopsis thaliana) receptor-like cytoplasmic kinase BOTRYTIS-INDUCED KINASE1 (BIK1) acts as a signaling hub of plant immunity. BIK1 homeostasis is maintained by a regulatory module in which CALCIUM-DEPENDENT PROTEIN KINASE28 (CPK28) regulates BIK1 turnover via the activities of two E3 ligases. Immune-induced alternative splicing of CPK28 attenuates CPK28 function. 


提出问题:However, it remained unknown whether CPK28 is under proteasomal control.


主要发现:Here, we demonstrate that CPK28 undergoes ubiquitination and 26S proteasome-mediated degradation, which is enhanced by flagellin treatment.


结果1-泛素连接酶ATL31/6与CPK28互作:Two closely related ubiquitin ligases, ARABIDOPSIS TÓXICOS EN LEVADURA31 (ATL31) and ATL6, specifically interact with CPK28 at the plasma membrane; this association is enhanced by flagellin elicitation. 


结果2-ATL31/6介导CPK28的泛素化与降解:ATL31/6 directly ubiquitinate CPK28, resulting in its proteasomal degradation.


结果3-ATL31/6介导BIK1的稳定性:Furthermore, ATL31/6 promote the stability of BIK1 by mediating CPK28 degradation.


结果4-ATL31/6介导植物免疫:Consequently, ATL31/6 positively regulate BIK1-mediated immunity.


结论:Our findings reveal another mechanism for attenuating CPK28 function to maintain BIK1 homeostasis and enhance immune responses.


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 摘 要 


模式识别受体PRRs识别到微生物分子模式后,会诱导免疫响应。拟南芥类受体胞质激酶BIK1作为植物免疫的信号中心发挥作用。BIK1内稳态是由一个调控模块所维持的,该模块中钙依赖性蛋白激酶CPK28通过两个E3连接酶的活性调控BIK1蛋白的周转。免疫诱导的CPK28基因可变剪切会减弱CPK28的功能。但是,对于CPK28是否受到泛素化的控制还不清楚。本文中,作者发现CPK28蛋白经历了泛素化和26S蛋白酶体介导的降解,该过程受到鞭毛蛋白处理的增强。两个近缘的泛素连接酶ATL31和ATL6会特异性地与CPK28蛋白在质膜上互作;该过程受到鞭毛蛋白诱导的增强。ATL31/6直接泛素化CPK28,导致其蛋白酶体降解。此外,ATL31/6通过介导CPK28的降解,促进BIK1的稳定性。最终,ATL31/6正向调控BIK1介导的免疫。本文的研究结果揭示了一种减弱CPK28功能,以维持BIK1内稳态,从而增强免疫响应的机制。


 通讯作者 

** 吕东平 **


个人简介:

1998年,内蒙古大学,学士;

2001年,中科院植物研究所,硕士;

2007年,美国夏威夷大学,博士;

2008年,夏威夷大学,博后;

2009-2011年,美国德克萨斯A&M大学,博后;

2011-2012年,美国德克萨斯A&M大学,助理研究科学家;

2012-至今,中科院遗传与发育生物学研究所,研究员。


研究方向植物抗病信号转导途径


doi: https://doi.org/10.1093/plcell/koab242


Journal: Plant Cell

Published dateOctober 01, 2021



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