For effective plant immunity, two defence mechanisms go hand in hand

Plants use two types of immune receptors to spot infections: receptors on the surface of the cell and receptors inside the cell. Cell-surface receptors detect pathogen-derived molecules that gather between plant cells, activating the plant’s first line of defence called pattern-triggered immunity (PTI). Intracellular receptors detect bacterial effector proteins that invade the plant’s host cells to suppress host defence mechanisms and help the pathogen to survive. The immunity activated in this case is called effector-triggered immunity (ETI).

Until now, researchers have mostly focused on PTI, namely immunity brought about by cell-surface receptors, rarely investigating that mediated only by intracellular receptors. Additionally, they haven’t managed to form a clear picture of interactions between these two defence mechanisms. Scientists supported by the EU-funded ImmunityByPairDesign and PERFECTION projects have found that each immune pathway acting on its own isn’t enough to provide effective resistance against bacteria. However, when both mechanisms are activated together, the bacterium is thwarted.

The research team achieved this breakthrough by studying ETI without inducing PTI. To do this, they engineered the model plant Arabidopsis thaliana, or mouse-ear cress, in order to use a chemical that would initiate the production of effector proteins inside the plant cells. The proteins were those of a pathogenic bacterium called Pseudomonas syringae. “Initially the inducible-effector system was generated to study ETI without interference from PTI. But what we saw at first didn’t make sense because ETI alone didn’t seem to do much. Then we re-introduced PTI back into the system and suddenly everything became clear,” remarked researcher Bruno Pok Man Ngou of projects’ host The Sainsbury Laboratory (TSL), United Kingdom, in an article posted on the TSL website.While the two distinct defence mechanisms were found to provide inadequate defence when acting on their own, when acting together they enhanced each other to provide strong resistance to the plant pathogen. More specifically, when cell-surface receptors recognise a pathogen, they activate multiple protein kinases and nicotinamide adenine dinucleotide phosphate (NADPH) oxidases – important components in a plant’s response to pathogen attacks. The team found that when intracellular receptors in turn detect the presence of pathogen effectors, they increase the abundance of protein kinases and NADPH oxidases through various mechanisms. Similarly, the hypersensitive ETI response that’s dependent on intracellular receptors is greatly enhanced through cell-surface receptor activation.

Senior scientist Prof. Jonathan Jones, also of TSL, stated: “It’s been a privilege to work with a wonderful team of co-authors on this important project. Ever since we distinguished defence activated by cell surface receptors and by intracellular receptors (PTI and ETI) 15 years ago, the questions of how these defences interact, and what ETI does in the absence of PTI, have remained open.”

This work will improve scientific understanding of plant immunity and help in the cultivation of stronger, more disease-resistant crops. The research findings have been published in the journal ‘Nature’.

PERFECTION (Probing mechanisms of pathogen effector recognition by plant Resistance proteins to elevate defence gene activation) ended in 2018. The 6-year ImmunityByPairDesign (Design and redesign of a plant immune receptor complex) project ends in September 2021.

For more information, please see:

ImmunityByPairDesign project

PERFECTION project