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Gentle, A.

Publications and source records attributed to Gentle, A..

2 recordsLinked to original sources

Computational design of de novo integrated domains enables rational control of pathogen effector recognition in plant NLR immune receptors.

The rapid evolution of plant pathogens poses a persistent threat to global agricultural sustainability, often outpacing the discovery and deployment of natural disease resistance genes. While bioengineering of plant intracellular immune receptors (NLRs) offers a potential solution, developing bespoke immune recognition remains constrained by the laborious characterisation of natural receptors and plant-pathogen interactions. Here, we describe a programmable framework that leverages generative AI protein design tools, RFdiffusion and ProteinMPNN, to design de novo integrated domains (IDs) against diverse pathogen effectors. By integrating these bespoke binders into the modular rice blast Pik-1/Pik-2 NLR receptor chassis, we successfully engineer recognition of a non-cognate virulence factor (effector) from the Panama disease pathogen, Fusarium oxysporum f. sp. cubense Tropical Race 4. Functional assays in Nicotiana benthamiana demonstrate that these de novo domains facilitate specific effector perception and initiate immune signalling, while structural and biophysical analyses confirm that de novo integrated domains maintain high structural fidelity to the initial designs and associate with their targets via the predicted interaction interfaces. Additionally, our findings provide orthogonal evidence for the role of integrated domains in regulation of NLR signalling, demonstrating integration of de novo IDs can either trigger autoactivity or, in some cases, lead to effector-mediated repression of cell death. By decoupling immune perception from natural evolutionary history through deploying AI-designed sensory domains, this work establishes a design-lead framework for generation of programmable plant immune receptors, providing a new avenue for bioengineering crops against emerging pathogens.

plant biology↗

The blast effector Pwl2 is a virulence factor that modifies the cellular localisation of host protein HIPP43 to suppress immunity.

The rice blast fungus Magnaporthe oryzae secretes a battery of effector proteins to facilitate host infection. Among these effectors, Pwl2 was first identified as a host specificity determinant for infection of weeping lovegrass (Eragrostis curvula) and is also recognised by the barley Mla3 resistance gene. However, its biological activity is not known. Here we show that PWL2 expression is regulated by the Pmk1 MAP kinase during cell-to-cell movement by M. oryzae at plasmodesmata (PD)-containing pit field sites. Consistent with its regulation, we provide evidence that Pwl2 binds to a barley heavy metal-binding isoprenylated protein HIPP43, which results in its displacement from plasmodesmata. Transgenic barley lines overexpressing either PWL2 or HIPP43 exhibit attenuated immune responses and increased disease susceptibility. By contrast, a Pwl2SNDEYWY mutant that does not interact with HIPP43, fails to alter the PD localisation of HIPP43. Targeted deletion of three copies of PWL2 in M. oryzae results in a{Delta} pwl2 mutant showing gain-of-virulence to weeping lovegrass and barley Mla3 lines, but also a reduction in severity of blast disease on susceptible host plants. Taken together, our results provide evidence that Pwl2 is a virulence factor that acts by suppressing host immunity through perturbing the plasmodesmatal deployment of HIPP43.

plant biology↗