Pull the fuzes: Processing protein precursors to generate apoplastic danger signals for triggering plant immunity.

Autor: Del Corpo D; Department of Biology and Biotechnology 'Charles Darwin,' Sapienza University of Rome, Rome, Italy., Coculo D; Department of Biology and Biotechnology 'Charles Darwin,' Sapienza University of Rome, Rome, Italy., Greco M; Department of Biology and Biotechnology 'Charles Darwin,' Sapienza University of Rome, Rome, Italy., De Lorenzo G; Department of Biology and Biotechnology 'Charles Darwin,' Sapienza University of Rome, Rome, Italy., Lionetti V; Department of Biology and Biotechnology 'Charles Darwin,' Sapienza University of Rome, Rome, Italy. Electronic address: vincenzo.lionetti@uniroma1.it.
Jazyk: angličtina
Zdroj: Plant communications [Plant Commun] 2024 Aug 12; Vol. 5 (8), pp. 100931. Date of Electronic Publication: 2024 Apr 30.
DOI: 10.1016/j.xplc.2024.100931
Abstrakt: The apoplast is one of the first cellular compartments outside the plasma membrane encountered by phytopathogenic microbes in the early stages of plant tissue invasion. Plants have developed sophisticated surveillance mechanisms to sense danger events at the cell surface and promptly activate immunity. However, a fine tuning of the activation of immune pathways is necessary to mount a robust and effective defense response. Several endogenous proteins and enzymes are synthesized as inactive precursors, and their post-translational processing has emerged as a critical mechanism for triggering alarms in the apoplast. In this review, we focus on the precursors of phytocytokines, cell wall remodeling enzymes, and proteases. The physiological events that convert inactive precursors into immunomodulatory active peptides or enzymes are described. This review also explores the functional synergies among phytocytokines, cell wall damage-associated molecular patterns, and remodeling, highlighting their roles in boosting extracellular immunity and reinforcing defenses against pests.
(Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE