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| Funder | Biotechnology and Biological Sciences Research Council |
|---|---|
| Recipient Organization | University of East Anglia |
| Country | United Kingdom |
| Start Date | Jan 01, 2021 |
| End Date | Dec 31, 2023 |
| Duration | 1,094 days |
| Number of Grantees | 1 |
| Roles | Principal Investigator |
| Data Source | UKRI Gateway to Research |
| Grant ID | BB/V002937/1 |
Just like humans, plants get sick. They can be infected by parasites as diverse as oomycetes, fungi, bacteria, viruses, nematode worms and insects. But, also like humans, plants have an immune system that helps them defend against disease. Their first line of defence are disease resistance genes. Many of these genes encode so-called immune receptors, which are proteins that detect parasites and kick-off the immune response.
Plant genomes may encode anywhere between 50 and 1000 immune receptors; some of which work solo as singletons, while others operate in pairs or as complex networks. One driving force behind the evolution of immune receptors is gene duplication. Receptor genes duplicate and afterwards the two copies can evolve in different ways.
The original immune receptors are multi-tasking proteins that detect parasites and trigger the immune response. Following gene duplication, evolution has led immune receptors to specialize. Some receptors became dedicated to pathogen detection and lost the ability to trigger a defence response on their own, whereas others operate in concert with these sensor receptors to trigger the immune response.
This project will study how a plant pathogen counteract an immune receptor network of its host plant. We will focus on the potato blight pathogen Phytophthora infestans and determine the mechanism by which it suppresses the function of the subset of immune receptors that trigger the immune response. Understanding the interplay between plant pathogens and their host's immune receptors would generate fundamental knowledge about the functioning principles that determine the outcomes of these interactions, which in turn would set the stage for researchers to be able to use them to protect agricultural crops from disease.
A better understanding of how these complex interactions between pathogens and plant immune receptor operate should set the stage for breeding crop plants that are better able to resist diseases. Our long-term aim is to understand the dynamics of plant-pathogen interactions in sufficient detail to improve our capacity to protect plants against crop diseases.
University of East Anglia
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