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Shoot 成熟增强了 FLS2 介导的对 的抗性。

Shoot Maturation Strengthens FLS2-Mediated Resistance to .

机构信息

Department of Plant Pathology, University of Georgia, Athens, GA 30602, U.S.A.

出版信息

Mol Plant Microbe Interact. 2023 Dec;36(12):796-804. doi: 10.1094/MPMI-02-23-0018-R. Epub 2023 Dec 22.

DOI:10.1094/MPMI-02-23-0018-R
PMID:37638673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10989731/
Abstract

Temporospatial regulation of immunity components is essential for properly activating plant defense response. Flagellin-sensing 2 (FLS2) is a surface-localized receptor that recognizes bacterial flagellin. The immune function of FLS2 is compromised in early stages of shoot development. However, the underlying mechanism for the age-dependent FLS2 signaling is not clear. Here, we show that the reduced basal immunity of juvenile leaves against pv. DC3000 is independent of FLS2. The flg22-induced marker gene expression and reactive oxygen species activation were comparable in juvenile and adult stages, but callose deposition was more evident in the adult stage than the juvenile stage. We further demonstrated that microRNA156, a master regulator of plant aging, does not influence the expression of and () but mildly suppresses callose deposition in juvenile leaves. Our experiments revealed an intrinsic mechanism that regulates the amplitude of FLS2-mediated resistance during aging. [Formula: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

摘要

免疫成分的时空调节对于植物防御反应的正常激活至关重要。鞭毛蛋白感应 2(FLS2)是一种位于表面的受体,可识别细菌鞭毛蛋白。在芽发育的早期阶段,FLS2 的免疫功能受损。然而,依赖于年龄的 FLS2 信号的潜在机制尚不清楚。在这里,我们表明,对 pv 的幼年叶片的基础免疫力降低。 DC3000 与 FLS2 无关。flg22 诱导的标记基因表达和活性氧的激活在幼叶和成年阶段相当,但与幼叶相比,成年阶段的胼胝质沉积更为明显。我们进一步证明,miRNA156 是植物衰老的主要调控因子,不影响 和 的表达(),但轻度抑制幼年叶片中胼胝质的沉积。我们的实验揭示了一种内在机制,可调节衰老过程中 FLS2 介导的抗性的幅度。[公式:见正文]版权所有 © 2023 作者。这是一个在 CC BY-NC-ND 4.0 国际许可下发布的免费开放文章。