Jurriaan Ton

Our lab investigates how plants employ their immune system to adapt to environmental stress (Wilkinson et al. 2019). Plants in relatively stress-free environments invest most of their resources in growth and reproduction. If plants live in hostile environments and are attacked by harmful microbes or insects, they activate inducible defence mechanisms. Activation of these defences is often costly, due to allocation of limited resources to defensive compounds, or toxicity of the defence response to the plant’s own metabolism. Plants are also capable of acquiring a less costly form of resistance, which can be activated after perception of environmental alarm signals that sensitise the plant’s immune system. This “defence priming” results in a faster and/or stronger defence reaction when the plant is attacked at a later stage.

We have a long-standing interest in the mechanisms by which priming-inducing chemicals, such beta-aminobutyric acid (BABA), are perceived in plants and trigger immune priming. This research has led to the discovery of the BABA receptor, which controls broad-spectrum disease resistance and plant growth via separate signalling pathways (Luna et al., 2014, Schwarzenbacher et al. 2020), and a novel structural analogue of BABA, R-beta-homoserine (RBH), which induces resistance in plants with fewer non-target effects on plant growth (Buswell et al. 2018).