4.8 Article

A secreted fungal subtilase interferes with rice immunity via degradation of SUPPRESSOR OF G2 ALLELE OF skp1

Journal

PLANT PHYSIOLOGY
Volume 190, Issue 2, Pages 1474-1489

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/plphys/kiac334

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Funding

  1. National Natural Science Foundation of China [32172372]
  2. Key Research & Development Program of Hubei Province [2021BBA236]
  3. Fundamental Research Funds for the Central Universities of China [2021ZKPY016]

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In this study, we identified a secreted fungal subtilase, UvPr1a, from the rice false smut fungus Ustilaginoidea virens, which interferes with rice immunity by degrading the rice protein OsSGT1, thereby promoting infection. This discovery provides tools for introducing resistance to rice false smut and deepens our understanding of plant-pathogen interactions.
Serine protease subtilase, found widely in both eukaryotes and prokaryotes, participates in various biological processes. However, how fungal subtilase regulates plant immunity is a major concern. Here, we identified a secreted fungal subtilase, UvPr1a, from the rice false smut (RFS) fungus Ustilaginoidea virens. We characterized UvPr1a as a virulence effector localized to the plant cytoplasm that inhibits plant cell death induced by Bax. Heterologous expression of UvPr1a in rice (Oryza sativa) enhanced plant susceptibility to rice pathogens. UvPr1a interacted with the important rice protein SUPPRESSOR OF G2 ALLELE OF skp1 (OsSGT1), a positive regulator of innate immunity against multiple rice pathogens, degrading OsSGT1 in a protease activity-dependent manner. Furthermore, host-induced gene silencing of UvPr1a compromised disease resistance of rice plants. Our work reveals a previously uncharacterized fungal virulence strategy in which a fungal pathogen secretes a subtilase to interfere with rice immunity through degradation of OsSGT1, thereby promoting infection. These genetic resources provide tools for introducing RFS resistance and further our understanding of plant-pathogen interactions.

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