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拟南芥 MIEL1 E3 连接酶通过促进 MYB96 的蛋白降解来负调控 ABA 信号通路。

The Arabidopsis MIEL1 E3 ligase negatively regulates ABA signalling by promoting protein turnover of MYB96.

机构信息

Department of Biological Sciences, Sungkyunkwan University, Suwon 16419, Republic of Korea.

出版信息

Nat Commun. 2016 Sep 12;7:12525. doi: 10.1038/ncomms12525.

DOI:10.1038/ncomms12525
PMID:27615387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5027273/
Abstract

The phytohormone abscisic acid (ABA) regulates plant responses to various environmental challenges. Controlled protein turnover is an important component of ABA signalling. Here we show that the RING-type E3 ligase MYB30-INTERACTING E3 LIGASE 1 (MIEL1) regulates ABA sensitivity by promoting MYB96 turnover in Arabidopsis. Germination of MIEL1-deficient mutant seeds is hypersensitive to ABA, whereas MIEL1-overexpressing transgenic seeds are less sensitive. MIEL1 can interact with MYB96, a regulator of ABA signalling, and stimulate its ubiquitination and degradation. Genetic analysis shows that MYB96 is epistatic to MIEL1 in the control of ABA sensitivity in seeds. While MIEL1 acts primarily via MYB96 in seed germination, MIEL1 regulates protein turnover of both MYB96 and MYB30 in vegetative tissues. We find that ABA regulates the expression of MYB30-responsive genes during pathogen infection and this regulation is partly dependent on MIEL1. These results suggest that MIEL1 may facilitate crosstalk between ABA and biotic stress signalling.

摘要

植物激素脱落酸(ABA)调节植物对各种环境挑战的反应。受控的蛋白质周转是 ABA 信号转导的一个重要组成部分。在这里,我们表明 RING 型 E3 连接酶 MYB30-INTERACTING E3 LIGASE 1(MIEL1)通过促进拟南芥中 MYB96 的周转来调节 ABA 敏感性。MIEL1 缺失突变体种子的萌发对 ABA 超敏感,而 MIEL1 过表达的转基因种子则不那么敏感。MIEL1 可以与 MYB96 相互作用,MYB96 是 ABA 信号转导的调节剂,并刺激其泛素化和降解。遗传分析表明,MYB96 在种子中对 ABA 敏感性的控制中对 MIEL1 是上位的。虽然 MIEL1 在种子萌发过程中主要通过 MYB96 起作用,但 MIEL1 在营养组织中也调节 MYB96 和 MYB30 的蛋白质周转。我们发现 ABA 在病原体感染过程中调节 MYB30 反应基因的表达,这种调节部分依赖于 MIEL1。这些结果表明,MIEL1 可能促进 ABA 和生物胁迫信号之间的串扰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/143b21f04a7c/ncomms12525-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/f0ff46b2df75/ncomms12525-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/b8c54a189632/ncomms12525-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/fec563955669/ncomms12525-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/1662254be8b4/ncomms12525-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/f6f011384fad/ncomms12525-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/143b21f04a7c/ncomms12525-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/f0ff46b2df75/ncomms12525-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/b8c54a189632/ncomms12525-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/fec563955669/ncomms12525-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/1662254be8b4/ncomms12525-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/f6f011384fad/ncomms12525-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28d5/5027273/143b21f04a7c/ncomms12525-f6.jpg

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