Biology subjects

Turley, E. K.

Publications and source records attributed to Turley, E. K..

4 recordsLinked to original sources

bioRxiv2026

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↗

bioRxiv2026

Colletotrichum higginsianum effector ChEC108 binds a plasmodesmal HMA protein and elicits plant defence

To establish infection, phytopathogens deploy effectors to compromise host defences and facilitate invasive growth. As part of this, the battle for control of symplastic connectivity via plasmodesmata is a key determinant of infection outcomes, yet little is known about how fungal effectors directly exploit these channels, and in turn, how hosts defend them. Here, we have identified ChEC108 as a plasmodesmal-targeting, cell-to-cell mobile effector from the anthracnose fungus, Colletotrichum higginsianum. ChEC108 binds the plasmodesmal protein HEAVY METAL-ASSOCIATED (HMA) ISOPRENYLATED PLANT PROTEIN 6 (HIPP6) from Arabidopsis via a tetrahedral metal ion coordination site with either of its HMA domains. Constitutive in planta expression of ChEC108 induces plasmodesmal closure and the upregulation of defence-associated genes in a manner dependent on its capacity to bind HIPP6. Further, HIPP6 binding impairs cell-to-cell mobility of ChEC108. Alongside the finding that loss of ChEC108 favoured C. higginsianum infection, this suggests ChEC108-HIPP6 interaction at plasmodesmata positively regulates defence.

plant biology↗

bioRxiv2026

Novel repressors of cambium activity in Arabidopsis

Wood is the greatest reservoir of terrestrial biomass and an essential carbon sink. Formed of xylem, it is derived from the cambium, a meristematic zone within plant stems from which phloem also forms. In Arabidopsis, cell division within the cambium is promoted by three major factors: auxin, cytokinin, and the TDIF-PXY ligand-receptor pair. Meristems and other stem cell populations are typically regulated by a balance between cell division-promoting factors and those that repress cell division to control meristem size, however few factors with cambium-repressing activity are known. Here we combined transcriptomics and transcriptional network analysis, which led to identification of related homeodomain zinc-finger transcription factors, ATHB23, ATHB30, and ATHB34, that repress cambium activity. These factors inhibit cambium activity by directly binding of promoters from a subset of auxin, cytokinin and TDIF-PXY transcriptional target genes, resulting in attenuation of their transcription. Our findings thus reveal a new mechanism underpinning balanced cambium activity.

plant biology↗

bioRxiv2024

A Necrotizing Toxin Promotes Pseudomonas syringae Infection Across Evolutionarily Divergent Plant Lineages

The Pseudomonas syringae species complex harbors a diverse range of plant pathogenic bacteria. While much of the current understanding of P. syringae is centered on interactions with flowering plants, much less is known about infection in evolutionarily divergent non-flowering lineages. Here, we took a comparative evolutionary approach to understand how P. syringae infects distantly related plants. We identify broad host P. syringae isolates causing significant disease in the liverwort Marchantia polymorpha, the fern Ceratopteris richardii, and the flowering plant Nicotiana benthamiana, which last shared a common ancestor over 500 million years ago. We demonstrate that phytotoxin enriched isolates belonging to the phylogroup 2 clade of the P. syringae species complex are particularly virulent in non-flowering plants, relying on a combination of type-3 secreted effector proteins and the lipopeptide phytotoxin syringomycin. The application of purified syringomycin promotes necrosis in diverse host tissues and activates conserved genes associated with redox regulation and cell death. Toxin-deficient phylogroups normally unable to infect Marchantia thalli exhibit enhanced bacterial growth when supplemented with exogenous syringomycin, further highlighting its role as a host-range defining factor in Pseudomonas. Collectively our research reveals a key role for the lipopeptide syringomycin in promoting Pseudomonas colonization, which works in concert with type-3 effector proteins to antagonize an exceptionally wide spectrum of land plants.

plant biology↗