Exquisite control of a plant immune pathway revealed
In a new study published in Nature, researchers working in the groups of Jijie Chai (Westlake University in Hangzhou, China) and Jane Parker (MPIPZ in Cologne, Germany) describe how Arabidopsis plants exert fine-control of a major immune signalling machinery rapid but restricted host cell death after pathogen recognition.
Seed-producing plants, including most crops, deploy large receptor families at the cell surface and inside cells to detect attack by diverse pathogenic microbes. Once activated, the receptors signal to conserved immune machineries which then induce defences that stop disease. A frequent outcome of specific pathogen recognition by intracellular receptors (called NLRs) is host cell death at sites of infection. While this sacrifices one or a few invaded cells, it rescues the rest of the plant to develop further and, in the case of crops, produce nutritious fruits and seeds. Pathogen-activated host cell death is therefore an important protective benefit to plants but, if not tightly controlled, can become a yield-reducing burdon.
In this Nature paper, Huang, Wang, Song, Jia and colleagues working in the groups of Jijie Chai (Westlake University in Hangzhou, China) and Jane Parker (MPIPZ in Cologne, Germany) describe how Arabidopsis plants exert fine-control of a major immune signalling machinery (called the EDS1-SAG101-NRG1 node), enabling rapid but restricted host cell death after pathogen recognition. Previous work had shown that Arabidopsis full-length (functional) NRG1 proteins (NRG1A and B), which are similar to some pathogen-sensing NLRs, are instead activated by host small molecules (SMs) generated downstream of pathogen detection. The SMs bind to and alter EDS1-SAG101 dimers so that they can associate with and activate NRG1A or B, leading to transcriptional reprogramming and cell death. In the Nature paper, the authors uncover the precise molecular mechanism by which NRG1A recognizes an SM-modified EDS1-SAG101 protein complex. Among EDS1-SAG101-NRG1A transcriptionally induced immunity genes is a truncated NRG1 protein variant (called NRG1C) which fails to signal because it lacks certain key domains. However, it effectively out-competes functional NRG1s by binding more strongly to the same surfaces created by SM-modified EDS1-SAG101.
Some important new insights into plant immunity regulation emerge from this study. First, restriction of host cell death by a competing non-functional plant component relies on initial defence and cell death mobilization by its functional counterparts – thereby creating a perfectly balanced homeostatic loop to confer resistance without severely compromising plant fitness. Second, the results show that pathogen- and ‘modified host’-activation of NLR immune receptors essentially work by the same molecular rules. These features help to rationally engineer NLRs for improved protection of crops against diseases.
