PubMed 34009359

PubMed ID: 34009359

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Stress memory gene FaHSP17.8-CII controls thermotolerance via remodeling PSII and ROS signaling in tall fescue.
Authors: Bi Aoyue, Wang Tao, Wang Guangyang, Zhang Liang, Wassie Misganaw, Amee Maurice, Xu Huawei, Hu Zhengrong, Liu Ao, Fu Jinmin, Chen Liang, Hu Tao
Journal: Plant physiology (Plant Physiol), Vol.187(3), 2021‑Nov‑03

DOI: 10.1093/plphys/kiab205 PMCID: PMC6327915

Abstract
High temperature is the most limiting factor in the growth of cool-season turfgrass. To cope with high-temperature stress, grass often adopt a memory response by remembering one past recurring stress and preparing a quicker and more robust reaction to the next stress exposure. However, little is known about how stress memory genes regulate the thermomemory response in cool-season turfgrass. Here, we characterized a transcriptional memory gene, Fa-heat shock protein 17.8 Class II (FaHSP17.8-CII) in a cool-season turfgrass species, tall fescue (Festuca arundinacea Schreb.). The thermomemory of FaHSP17.8-CII continued for more than 4 d and was associated with a high H3K4me3 level in tall fescue under heat stress (HS). Furthermore, heat acclimation or priming (ACC)-induced reactive oxygen species (ROS) accumulation and photosystem II (PSII) electron transport were memorable, and this memory response was controlled by FaHSP17.8-CII. In the fahsp17.8-CII mutant generated using CRISPR/Cas9, ACC+HS did not substantially block the ROS accumulation, the degeneration of chloroplast ultra-structure, and the inhibition of PSII activity compared with HS alone. However, overexpression of FaHSP17.8-CII in tall fescue reduced ROS accumulation and chloroplast ultra-structure damage, and improved chlorophyll content and PSII activity under ACC+HS compared with that HS alone. These findings unveil a FaHSP17.8-CII-PSII-ROS module regulating transcriptional memory to enhance thermotolerance in cool-season turfgrass.
Publication Types
Journal Article Research Support, Non-U.S. Gov't
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