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钙调素结合蛋白 60b 在植物免疫中发挥双重作用。

CALMODULIN-BINDING PROTEIN 60b plays dual roles in plant immunity.

机构信息

Department of Botany, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.

Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.

出版信息

Plant Commun. 2021 Jun 17;2(6):100213. doi: 10.1016/j.xplc.2021.100213. eCollection 2021 Nov 8.

Abstract

SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1 (SARD1) and CALMODULIN-BINDING PROTEIN 60g (CBP60g) are two master transcription factors that regulate many defense-related genes in plant immunity. They are required for immunity downstream of the receptor-like protein SUPPRESSOR OF NPR1-1, CONSTITUTIVE 2 (SNC2). Constitutive defense responses in the gain-of-function autoimmune mutant are modestly affected in either or single mutants but completely suppressed in the double mutant. Here we report that CBP60b, another member of the CBP60 family, also functions as a positive regulator of SNC2-mediated immunity. Loss-of-function mutations of suppress the constitutive expression of and enhanced disease resistance in , whereas overexpression of leads to elevated expression and constitutive defense responses. In addition, transient expression of in activates the expression of the :: reporter gene. Chromatin immunoprecipitation assays further showed that CBP60b is recruited to the promoter region of , suggesting that it directly regulates expression. Interestingly, knocking out in the wild-type background leads to ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)-dependent autoimmunity, suggesting that CBP60b is required for the expression of a guardee/decoy or a negative regulator of immunity mediated by receptors carrying an N-terminal Toll-interleukin-1 receptor-like domain.

摘要

系统性获得性抗性缺陷 1(SARD1)和钙调素结合蛋白 60g(CBP60g)是两种调节植物免疫中许多防御相关基因的主要转录因子。它们是受体样蛋白 SUPPRESSOR OF NPR1-1、CONSTITUTIVE 2(SNC2)下游免疫所必需的。在功能获得性自身免疫突变体中,组成性防御反应在 或 单个突变体中受到适度影响,但在 双突变体中完全受到抑制。在这里,我们报告另一种 CBP60 家族成员 CBP60b 也作为 SNC2 介导免疫的正调节剂发挥作用。 的功能丧失突变 抑制 和 在 中的组成性表达和增强的疾病抗性,而 的过表达导致 表达升高和组成性防御反应。此外, 在 中的瞬时表达激活了 :: 报告基因的表达。染色质免疫沉淀测定进一步表明,CBP60b 被招募到 的启动子区域,表明它直接调节 表达。有趣的是,在野生型背景中敲除 会导致 EDS1 依赖性自身免疫,这表明 CBP60b 是携带 N 端 Toll-白细胞介素-1 受体样结构域的受体介导的免疫的看守/诱饵或负调节剂表达所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6540/8577148/732f4389f419/gr1.jpg

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