Plant perception of β-aminobutyric acid is mediated by an aspartyl-tRNA synthetase

E. Luna, M. Van Hulten, Y. Zhang, Oliver Berkowitz, A. López, P. Pétriacq, M.A. Sellwood, B. Chen, M.M. Burrell, A.M.L. Van De Meene, C.M.J. Pieterse, V. Flors, J. Ton

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Abstract

Specific chemicals can prime the plant immune system for augmented defense. β-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 noncanonical defense signaling in the cytoplasm after pathogen attack. This priming was associated with aspartic acid accumulation and tRNA-induced phosphorylation of translation initiation factor eIF2α. However, mutation of eIF2α-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. © 2014 Nature America, Inc. All rights reserved.
Original languageEnglish
Pages (from-to)450-456
JournalNature Chemical Biology
Volume10
Issue number6
DOIs
Publication statusPublished - 2014

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