Xyloglucan endotransglucosylase/hydrolase gene TaXTH3A promotes resistance to Fusarium crown rot in wheat

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Authors: Shufa Zhang, Linrun Xiang, Li Zhao, Xinhao Nie, Xingxia Geng, Jiaojiao Guo, Jianmin Wu, Xinhong Chen, Yi-Xiang Wang
Cited by: 1
References: 70

Abstract

Fusarium crown rot (FCR), primarily caused by Fusarium pseudograminearum and other Fusarium species, is a devastating wheat disease that has led to substantial yield losses worldwide. In this study, a xyloglucan endotransglucosylase/hydrolase gene, TaXTH3A associated with FCR resistance was identified by integrating bulked segregant exome capture sequencing (BSE-Seq) and transcriptome sequencing (RNA-Seq) analyses. Functional characterization revealed that TaXTH3A encodes a secreted protein localized to the cell wall, demonstrated by a yeast signal sequence trap system and subcellular localization assays. Transgenic validation confirmed that TaXTH3A overexpression significantly enhances FCR resistance, accompanied by reduced H 2 O 2 accumulation, increased catalase activity, and improved disease resistance. Transcriptome profiling further indicated that TaXTH3A regulates the expression of genes involved in plant defense and xyloglucan metabolism during F . pseudograminearum infection. Furthermore, TaXTH3A -overexpressing lines exhibited increased xyloglucan endotransglucosylase (XET) activity and elevated hemicellulose content in leaf sheaths upon infection. Collectively, these findings suggest that, TaXTH3A enhances wheat resistance to F . pseudograminearum by regulating cell wall remodeling and associated defense responses. This study provides new insights into the molecular mechanisms underlying FCR resistance and offers a potential target for the genetic improvement of disease-resistant wheat cultivars.

Fields of Study & Subjects

Polysaccharides and Plant Cell Walls Mycotoxins in Agriculture and Food Plant-Microbe Interactions and Immunity

Publication details

Journal / source
Journal of Integrative Agriculture
Publisher
Elsevier BV
Publication date
1 June 2026
Language
EN