A new study reveals how certain proteins associate into distinct signalling modules to orchestrate the plant defence response.
Plant disease resistance depends on recognition of pathogen molecules, followed by activation of defence mechanisms. Scientists are trying to understand the complex cellular mechanisms that are activated when a pathogen interacts with a recognising protein (“receptor”) in a plant cell. Key components of these important processes have been defined using genetics, genomics and proteomics, and researchers are now drilling down into how these cellular components work together.
While much research has focused on how plants recognise pathogen molecules, much less is known about the events that convert recognition into defence.
Plant cells carry multiple and diverse immune receptors which recognise pathogen virulence factors. These receptors are usually nucleotide-binding, leucine-rich repeat (NLR) proteins. Most NLRs act as sensors, but some act as “helper” NLRs, often of the RPW8-like NLR (RNL) family, that support sensor NLR signalling. Many sensor NLRs also require EDS1 family proteins for signalling. For decades we have known that RNL and EDS1 families must be present for immune signalling, but how and why they are needed has remained a mystery.
Scientists at The Sainsbury Laboratory and the Max Planck Institute for Plant Breeding Research set out to answer these questions. In a recent article published in Nature Communications, the researchers found that RNLs NRG1 and ADR1 form two distinct signalling modules with the EDS1-family members EDS1-SAG101 or EDS1-PAD4, respectively. Furthermore, the association between NRG1 with EDS1-SAG101 only occurs upon effector recognition by sensor NLRs. While a previous genetic study had shown that the presence of both families was required, this study confirms that they form specific associations upon immune activation to orchestrate a defence response.
The genes for these components are deeply conserved across plants, which makes these findings potentially relevant to all flowering plants. This core discovery about plant immunity informs the engineering of NLRs and the components required to develop robust disease resistance in plants.
Dr Joanna Feehan, co-first author based at The Sainsbury Laboratory, said “It’s exciting to discover that these core immune signalling components are working together in plant defence. The next step will be uncovering how they work together, and what exactly they do to restrict pathogens.”
Prof. Jonathan Jones, co-author and group leader at The Sainsbury Laboratory, said “Plants carry an enormous diversity in their capacity to detect and respond to different pathogen molecules. To move recognition capacity from one plant to another in the interests of controlling crop disease, we may need to also move any potentially required signalling components, and that is why fundamental understanding of these signalling mechanisms is so important. It’s been a pleasure to work the Parker lab on this, a collaboration initiated at the last big pre-COVID conference in our field in Glasgow 2019, which illustrates why scientific conferences are so important”
The paper “Pathogen effector recognition-dependent association of NRG1 with EDS1 and SAG101 in TNL receptor immunity” can be viewed online at http://www.nature.com/ncomms under the DOI 10.1038/s41467-021-23614-x.
The press release from the Max Planck Institute can be found here.
This project was co-led by Professor Jane Parker and co-authored by Dr Xinhua Sun and Dr Dimitry Lapin at the Max Planck Institute. Their work was supported by the Max-Planck Society and Deutsche Forschungsgemeinschaft grants SFB 680 and SFB-1403–414786233; DFG-ANR Trilateral “RADAR” grant and a Chinese Scholarship Council doctoral fellowship. Joanna Feehan’s PhD work was supported by a core grant from the Gatsby Charitable foundation to TSL.
For more information or to request an interview with Jonathan Jones or Joanna Feehan, please contact Mia Cerfonteyn at email@example.com.