1. The rice E3 ubiquitin ligase-transcription factor module targets two trypsin inhibitors to enhance broad-spectrum disease resistance.
- Author
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Zhang C, Fang H, Wang J, Tao H, Wang D, Qin M, He F, Wang R, Wang GL, and Ning Y
- Subjects
- Transcription Factors metabolism, Transcription Factors genetics, Plant Immunity, Plants, Genetically Modified, Magnaporthe, Oryza microbiology, Oryza metabolism, Oryza genetics, Disease Resistance genetics, Plant Proteins metabolism, Plant Proteins genetics, Plant Diseases microbiology, Plant Diseases immunology, Ubiquitin-Protein Ligases metabolism, Ubiquitin-Protein Ligases genetics, Gene Expression Regulation, Plant, Xanthomonas pathogenicity, Trypsin Inhibitors metabolism, Trypsin Inhibitors pharmacology
- Abstract
Broad-spectrum disease resistance (BSR) is crucial for controlling plant diseases and relies on immune signals that are subject to transcriptional and post-translational regulation. How plants integrate and coordinate these signals remains unclear. We show here that the rice really interesting new gene (RING)-type E3 ubiquitin ligase OsRING113 targets APIP5, a negative regulator of plant immunity and programmed cell death (PCD), for 26S proteasomal degradation. The osring113 mutants in Nipponbare exhibited decreased BSR, while the overexpressing OsRING113 plants showed enhanced BSR against Magnaporthe oryzae (M. oryzae) and Xanthomonas oryzae pv. oryzae (Xoo). Furthermore, APIP5 directly suppressed the transcription of the Bowman-Birk trypsin inhibitor genes OsBBTI5 and AvrPiz-t-interacting protein 4 (APIP4). Overexpression of these two genes, which are partially required for APIP5-mediated PCD and disease resistance, conferred BSR. OsBBTI5 and APIP4 associated with and stabilized the pathogenesis-related protein OsPR1aL, which promotes M. oryzae resistance. Our results identify an immune module with integrated and coordinated hierarchical regulations that confer BSR in plants., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)
- Published
- 2024
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