Current methods of pest and disease control in tomato, Solanum lycopersicum, depend largely on chemical pesticides and/or single resistance genes. The use of plant defence activators would provide an alternative method to control pests and diseases. However, previous attempts to exploit this approach resulted in undesirable side effects on plant growth, and did not address durability of the induced protection.
We have developing protocols to reduce tomato disease by means of defence priming without major yield penalties. These strategies aim to obtain long-lasting disease protection against commercially relevant tomato pathogens, such as Botrytis cinerea.
In a joint project with our collaborators from the University of Lancaster (1), current research is focusing on the optimization of seed and seedling treatments of tomato, ultimately aiming to integrate these priming treatments with conventional methods of disease protection, such as multigenic cultivar resistance and fungicide applications. We have recently identified commercially feasible application methods of beta-aminobutyruic acid (BABA) and jasmonic acid (JA), which induce durable disease resistance in tomato without concurrent impacts on plant growth or colonization by plant-beneficial microbes (2).
As a result of our research on the onset of defence priming in Arabidopsis, we are investigating whether the benefits of BABA-induced defence priming can be separated from the associated stress reaction to this agent. The protective benefits of BABA are well-documented for tomato. BABA induces resistance in tomato against a wide range of commercially important diseases, such as Botrytis cinerea (2), Phytophthora infestans (3), Fusarium oxysporum fsp. Lycopersici (4) and Clavibacter michiganensis (5). From work with our model plant Arabidopsis, we know that over-expression of the BABA receptor gene IBI1 increases basal resistance and resistance responsiveness to BABA, while reducing BABA-induced growth repression (6). We are currently working with industrial partners to exploit this knowledge and enhance crop protection with minimal side-effects on plant growth and reproduction. Furthermore, our understanding of the molecular interaction between BABA and its receptor has allowed us to design chemical analogues of BABA that are faster metabolized by the plant, and therefore less repressive on plant growth.
1. Worrall et al. (2012) New Phytologist, 193 (3). pp. 770-778. 2. Luna, L., et al. (2015). Plant Disease (in press). 3. Cohen, et al, (1994) Plant Physiology, 104, 59-66. 4. Cohen, Y. (2002) Plant Disease, 86, 448-157. 5. Baysal et al (2005) European Journal of Plant Pathology, 112, 361-369. 6. Luna et al. (2014) Nature Chemical Biology. 10: 450-456.