Biology subjects

Schol, C. R.

Publications and source records attributed to Schol, C. R..

3 recordsLinked to original sources

bioRxiv2026

Effector-centred proximity-dependent labelling enables the discovery of cell-surface immune receptors in plants

Identifying plant disease resistance proteins remains challenging, particularly for cell-surface receptors that perceive apoplastic pathogen effectors through transient or indirect interactions. Here, we establish effector-centred proximity-dependent labelling using TurboID as a protein-level approach to identify immune receptors and guarded host targets in planta. We fused three apoplastic effectors, Avr2 and Avr4 from Fulvia fulva and XEG1 from Phytophthora sojae, to TurboID and transiently expressed these fusion proteins in leaves of Nicotiana benthamiana and tomato (Solanum lycopersicum). The fusions significantly biotinylate their matching receptors, including Cf-4 by Avr4-TurboID and Cf-2 by Avr2-TurboID, as well as the guarded virulence target of Avr2, the Rcr3 protease, demonstrating that both direct and indirect recognition systems can be captured. Application of this approach to XEG1 revealed SlEix1 as the functional ortholog of NbRXEG1. Functional assays and structural modelling support SlEix1 as a signalling-competent receptor contributing to XEG1-triggered immunity. Together with previous studies, these findings position the tomato EIX locus as a multi-effector immune hub encoding closely related receptor-like proteins with distinct ligand specificities. Collectively, this study establishes effector-TurboID-mediated proximity-dependent labelling as a versatile approach for identifying cell surface plant immune receptors and apoplastic virulence targets, providing a scalable route to accelerate resistance gene discovery in crop species.

plant biology↗

bioRxiv2025

Mutation or deletion of the Avr6 avirulence effector gene of Fulvia fulva leads to breakdown of the Cf-6 leaf mold resistance locus in tomato

Genetic resistance mediated by Cf cell-surface receptors is a cornerstone of tomato breeding against leaf mold disease caused by the fungal pathogen Fulvia fulva. After widespread deployment of the Cf-9 resistance locus, breeders increasingly relied on Cf-6, yet Cf-6-mediated resistance has already been overcome in multiple regions. The molecular basis of this breakdown, and the identity of the matching avirulence (Avr) effector, have remained unresolved. Here, we use comparative genomics and functional genetics to identify the F. fulva effector Avr6 as the previously described apoplastic protein Ecp5. Sequencing of Cf-6-breaking strains revealed either deletion of the Ecp5 locus or non-synonymous mutations in its coding sequence. Using transient expression, targeted gene knockout, and complementation assays, we show that Ecp5 is both necessary and sufficient for Cf-6-mediated recognition and defence activation. We then use Avr6-triggered cell death as a phenotypic marker in a bulked segregant analysis combined with Comparative Subsequence Sets analysis (CoSSa) to map Cf-6 to a [~]2 Mb interval on the short arm of chromosome 12 that overlaps the previously described Cf-Ecp5.12 locus. Sequencing of Avr6 in a broad strain collection reveals a predominantly conserved allele under apparent purifying selection, with recent independent loss-of-function variants in Europe and South America that confer virulence on Cf-6 plants. Together, these findings establish the Avr6-Cf-6 gene-for-gene pair, explain the erosion of Cf-6-mediated resistance, and illustrate how effector loss or mutation provides a rapid route for F. fulva adaptation, with important implications for designing more durable resistance strategies against tomato leaf mold.

microbiology↗

bioRxiv2023

Sequential breakdown of the complex Cf-9 leaf mould resistance locus in tomato by Fulvia fulva

O_LILeaf mould, caused by Fulvia fulva, is a devastating disease of tomato plants. In many commercial tomato cultivars, resistance to this disease is governed by the Cf-9 locus, which comprises five paralogous genes (Cf-9A-9E) that encode receptor-like proteins. Two of these proteins contribute to resistance: Cf-9C recognizes the previously identified F. fulva effector Avr9 and provides resistance during all plant growth stages, while Cf-9B recognises the yet-unidentified F. fulva effector Avr9B and provides mature plant resistance only. In recent years, F. fulva strains have emerged that have overcome the Cf-9 locus, with Cf-9C circumvented through Avr9 deletion. To understand how Cf-9B is circumvented, we set out to identify Avr9B. C_LIO_LIComparative genomics, in planta transient expression assays and gene complementation experiments were used to identify Avr9B, while gene sequencing was used to assess Avr9B allelic variation across a worldwide strain collection. C_LIO_LIA strict correlation between Avr9 deletion and resistance-breaking mutations in Avr9B was observed in strains recently collected from Cf-9 cultivars, whereas Avr9 deletion but no mutations in Avr9B were observed in older strains. C_LIO_LIThis research showcases how F. fulva has evolved to sequentially break down the two functional resistance genes of the complex Cf-9 locus and highlights that this locus now has limited value for controlling leaf mould disease in worldwide commercial tomato production. C_LI

microbiology↗