Chinese Bulletin of Botany ›› 2026, Vol. 61 ›› Issue (5): 821-833.DOI: 10.11983/CBB25107  cstr: 32102.14.CBB25107

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Overexpression of ATG8i Enhances Disease Resistance in Arabidopsis

Wang Wenxu, Zhao Yating, Lan Hujiao, Zhao Huanting1, Zhang Rui1, Liu Jianzhong1,2,*   

  1. 1College of Life Sciences, Zhejiang Normal University, Jinhua 321004, China;
    2Zhejiang Provincial Key Laboratory of Biotechnology on Specialty Economic Plants, College of Life Sciences, Zhejiang Normal University, Jinhua 321004, China
  • Received:2025-06-10 Accepted:2025-10-28 Published:2025-11-05
  • Contact: *E-mail: jzliu@zjnu.cn
  • About author:† These authors contributed equally to this paper

Abstract: INTRODUCTION: Autophagy is an evolutionarily conserved catabolic process that degrade damaged or unwanted cellular materials including organelles, macromolecules and even pathogens. AUTOPHAGY RELATED GENE 8 (ATG8) proteins play critical roles in autophagy. There are 9 ATG8 isoforms in Arabidopsis that are grouped into two clades. ATG8h and ATG8i are categorized into clade II because of their unique features. However, their functions in resistance against biotrophic and necrotrophic pathogens are not fully understood.
RATIONALE: Our previous study revealed that simultaneous knockout of ATG8h and ATG8i enhanced Arabidopsis resistance to the biotrophic fungal pathogen Golovinomyces cichoracearum. However, neither the role of this gene in resistance to biotrophic bacterial pathogen and necrotrophic fungal pathogen nor the effect of its overexpression on disease resistance has been investigated previously.
RESULTS: To further understand the roles of ATG8i in resistance against both biotrophic bacterial pathogen and necrotrophic fungal pathogens, the ATG8i overexpressing Arabidopsis lines driven by 35S promoter were generated. The generated ATG8i overexpressing lines exhibited an elevated resistance to the biotrophic bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (PstDC3000), but displayed an increased susceptibility to a toxin secreted by necrotrophic fungal pathogen. The enhanced resistance to the biotrophic pathogen was associated with the increased expression of Pathogenesis-related (PR) gene, elevated accumulation of H2O2 and enhanced callose deposition, whereas the increased sensitivity to the necrotrophic fungal toxin was associated with the significantly reduced expression of the genes in jasmonic acid (JA) pathway.
CONCLUSION: Based on the results reported here together with our previously published results, we conclude that either overexpression or loss of ATG8i function can activate resistance to biotrophic pathogens, but reduce the resistance to necrotrophic pathogens. Overexpression of ATG8i appears to activate salicylic acid (SA)-mediated resistance but suppress JA-mediated resistance.

Key words: autophagy, autophagy-related gene, disease resistance, biotrophic pathogen, necrotropic pathogen