期刊
NATURE CHEMICAL BIOLOGY
卷 10, 期 6, 页码 450-456出版社
NATURE PORTFOLIO
DOI: 10.1038/NCHEMBIO.1520
关键词
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资金
- VENI grant from the Netherlands Organisation of Scientific Research (NWO) [863.04.019]
- Biotechnology and Biological Sciences Research Council Institute [BB/E023959/1]
- European Research Council [309944-Prime-A-Plant]
- Leverhulme Trust [RL-2012-042]
- European Union Seventh Framework Programme [265865-PURE]
- Felix Thornley Cobbold Agricultural Trust
- VICI grant from NWO [865.04.002]
- BBSRC [BB/E023959/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/E023959/1] Funding Source: researchfish
Specific chemicals can prime the plant immune system for augmented defense. beta-aminobutyric acid (BABA) is a priming agent that provides broad-spectrum disease protection. However, BABA also suppresses plant growth when applied in high doses, which has hampered its application as a crop defense activator. Here we describe a mutant of Arabidopsis thaliana that is impaired in BABA-induced disease immunity (ibi1) but is hypersensitive to BABA-induced growth repression. IBI1 encodes an aspartyl-tRNA synthetase. Enantiomer-specific binding of the R enantiomer of BABA to IBI1 primed the protein for non-canonical defense signaling in the cytoplasm after pathogen attack. This priming was associated with aspartic acid accumulation and tRNA-induced phosphorylation of translation initiation factor elF2 alpha. However, mutation of elF2 alpha-phosphorylating GCN2 kinase did not affect BABA-induced immunity but relieved BABA-induced growth repression. Hence, BABA-activated IBI1 controls plant immunity and growth via separate pathways. Our results open new opportunities to separate broad-spectrum disease resistance from the associated costs on plant growth.
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