期刊
NATURE PLANTS
卷 6, 期 8, 页码 1008-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41477-020-0724-1
关键词
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资金
- NSF CAREER Award [1943591]
- Hellman Foundation Fellowship
- UC San Diego Start-up funds
- Ciencias sem Fronteiras/CNPq fellowship [200260/2015-4]
- Cell and Molecular Genetics (CMG) Training Program at the University of California, San Diego
- NSF [1546899]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1943591] Funding Source: National Science Foundation
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [1546899] Funding Source: National Science Foundation
The survival of all living organisms requires the ability to detect attacks and swiftly counter them with protective immune responses. Despite considerable mechanistic advances, the interconnectivity of signalling modules often remains unclear. A newly characterized protein, IMMUNOREGULATORY RNA-BINDING PROTEIN (IRR), negatively regulates immune responses in both maize andArabidopsis, with disrupted function resulting in enhanced disease resistance. IRR associates with and promotes canonical splicing of transcripts encoding defence signalling proteins, including the key negative regulator of pattern-recognition receptor signalling complexes, CALCIUM-DEPENDENT PROTEIN KINASE 28 (CPK28). On immune activation by Plant Elicitor Peptides (Peps), IRR is dephosphorylated, disrupting interaction withCPK28transcripts and resulting in the accumulation of an alternative splice variant encoding a truncated CPK28 protein with impaired kinase activity and diminished function as a negative regulator. We demonstrate a new mechanism linking Pep-induced post-translational modification of IRR with post-transcriptionally mediated attenuation of CPK28 function to dynamically amplify Pep signalling and immune output. A newly identified RNA-binding protein is dephosphorylated after immunity-induced Pep1 perception inArabidopsisand maize. This modification induces alternative splicing-mediated production of a truncated CPK28 kinase with reduced activity, which increases PEPR signalling capacity.
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