Regulatory networks of senescence‐associated gene‐transcription factors promote degradation in Moso bamboo shoots

Author:

Zhang Wenyu1ORCID,Shi Man1,Yang Kebin2,Zhang Junbo1,Gao Zhimin3,El‐Kassaby Yousry A.4,Li Quan1,Cao Tingting1,Deng Shixin1,Qing Hongsheng1,Wang Zhikang1ORCID,Song Xinzhang1ORCID

Affiliation:

1. State Key Laboratory of Subtropical Silviculture Zhejiang A&F University Hangzhou China

2. College of Landscape Architecture and Forestry Qingdao Agricultural University Qingdao China

3. International Center for Bamboo and Rattan Beijing China

4. Department of Forest and Conservation Sciences, Faculty of Forestry, Forest Sciences Centre University of British Columbia Vancouver British Columbia Canada

Abstract

AbstractBamboo cultivation, particularly Moso bamboo (Phyllostachys edulis), holds significant economic importance in various regions worldwide. Bamboo shoot degradation (BSD) severely affects productivity and economic viability. However, despite its agricultural consequences, the molecular mechanisms underlying BSD remain unclear. Consequently, we explored the dynamic changes of BSD through anatomy, physiology and the transcriptome. Our findings reveal ruptured protoxylem cells, reduced cell wall thickness and the accumulation of sucrose and reactive oxygen species (ROS) during BSD. Transcriptomic analysis underscored the importance of genes related to plant hormone signal transduction, sugar metabolism and ROS homoeostasis in this process. Furthermore, BSD appears to be driven by the coexpression regulatory network of senescence‐associated gene transcription factors (SAG‐TFs), specifically PeSAG39, PeWRKY22 and PeWRKY75, primarily located in the protoxylem of vascular bundles. Yeast one‐hybrid and dual‐luciferase assays demonstrated that PeWRKY22 and PeWRKY75 activate PeSAG39 expression by binding to its promoter. This study advanced our understanding of the molecular regulatory mechanisms governing BSD, offering a valuable reference for enhancing Moso bamboo forest productivity.

Publisher

Wiley

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