The response of Arabidopsis to the chemical defence activator ß-aminobutyric acid (BABA) has emerged as a model system to study the molecular mechanisms underpinning defence priming. BABA primes multiple defence responses that are controlled by different defence signalling pathways (1-3). BABA has long been known for its protective effects against plant disease, including devastating crop diseases such as late blight, downy mildew and grey mould (4). However, plant immunization by BABA is often associated with undesirable side effects, causing substantial repression of plant growth. These costs have hampered application of the chemical in crop protection schemes.
We recently identified and characterized the impaired in BABA-induced immunity 1 (ibi1) mutant of Arabidopsis, which was selected for loss of BABA-induced resistance against downy mildew (6). This mutant is impaired in BABA-induced priming against biotrophic and necrotrophic pathogens, but develops exaggerated stress symptoms upon application of high doses of the agent.
Identification of the IBI1 gene revealed that the corresponding protein, an aspartyl tRNA-synthetase (AspRS), acts as a receptor of BABA (6). We demonstrated that binding of the R-enantiomer of BABA to the aspartic acid-binding pocket of IBI1 blocks the default AspRS activity of IBI1, thereby priming a secondary (‘non-canonical‘) defence function of the protein that becomes active in the cytoplasm after subsequent pathogen attack. Importantly, this study also revealed that the undesirable side effects of the BABA, i.e. plant growth repression, are controlled by a separate stress pathway. The stress response is triggered by uncharged tRNA, which increases in cells of BABA-treated plants due to the AspRS-blocking activity of the chemical. The uncharged tRNA activates the protein kinase GCN2, which in turn represses mRNA translation causing plant stress (6).
The discovery of the IBI1 receptor has provided us with exciting opportunities to uncouple the broad-spectrum resistance response from the associated stress response. Considering that BABA augments multigenic resistance, and provides hands-on tools to deliver sustainable crop protection against diseases that are difficult to control by single resistance genes or fungicides, such as downy mildew and late blight.
Current research in the lab focuses on the characterization of the downstream signalling pathways of IBI1. Using transcriptomic and metabolomic approaches, combined with genome-wide screens for IBI1-interacting proteins, we have identified new signalling steps regulating the IBI1-dependent priming of cell wall defence (Schwarzenbacher & Ton, unpublished results). Furthermore, we have recently discovered a new priming agent, R-beta-homoserine (RBH), which, unlike BABA, induces broad-spectrum resistance in Arabidopsis without reductions in plant growth (7). Despite its structural similarity to BABA, this molecule primes partially different signalling pathways than BABA (7). Currently, we are conducting forward genetic screens to identify new signalling components in the pathways controlling RBH-induced priming in Arabidopsis.
1. Ton J & Mauch-Mani B (2004) Plant J. 38, 119-130 2. Ton J. et al. (2005) Plant Cell 17, 987-999. 3. Van der Ent S et al. & Ton J (2009) New Phytol. 183, 419-431. 4. Cohen YR (2002) Plant Disease 86: 448-457. 5. Van Hulten et al. & Ton J. PNAS 103: 5602-5607. 6. Luna E. et al & Ton J (2014) Nat. Chem Biol. 10: 450-456. 7. Buswell et al. & Ton J (2018) New Phyt 218: 1205-1216.