:Regulation of NLR stability in plant immunity论文

:Regulation of NLR stability in plant immunity论文

本文主要研究内容

作者(2019)在《Regulation of NLR stability in plant immunity》一文中研究指出:Plant nucleotide binding domain and leucinerich repeat(NLR) receptors recognize pathogen effectors directly or indirectly and mediate innate immune responses. NLR-mediated immunity also has direct impacts on plant growth and development, as well as yield and survival. The levels of NLR proteins are therefore intricately controlled in plants to balance defense responses and other processes. In recent years, the ubiquitination-26 S proteasome system and the HSP90 chaperones have emerged as having key functions in the regulation of NLR stability. The N-end rule pathway of protein degradation is also directly linked to NLR stability.Recent progress in the regulation of NLR stability and turnover is summarized here, focusing on the key components and pathways.

Abstract

Plant nucleotide binding domain and leucinerich repeat(NLR) receptors recognize pathogen effectors directly or indirectly and mediate innate immune responses. NLR-mediated immunity also has direct impacts on plant growth and development, as well as yield and survival. The levels of NLR proteins are therefore intricately controlled in plants to balance defense responses and other processes. In recent years, the ubiquitination-26 S proteasome system and the HSP90 chaperones have emerged as having key functions in the regulation of NLR stability. The N-end rule pathway of protein degradation is also directly linked to NLR stability.Recent progress in the regulation of NLR stability and turnover is summarized here, focusing on the key components and pathways.

论文参考文献

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  • 论文详细介绍

    论文作者分别是来自Frontiers of Agricultural Science and Engineering的,发表于刊物Frontiers of Agricultural Science and Engineering2019年02期论文,是一篇关于,Frontiers of Agricultural Science and Engineering2019年02期论文的文章。本文可供学术参考使用,各位学者可以免费参考阅读下载,文章观点不代表本站观点,资料来自Frontiers of Agricultural Science and Engineering2019年02期论文网站,若本站收录的文献无意侵犯了您的著作版权,请联系我们删除。

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