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A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch

Lukas Meile, View ORCID ProfileDaniel Croll, Patrick C. Brunner, Clémence Plissonneau, Fanny E. Hartmann, Bruce A. McDonald, Andrea Sánchez-Vallet
doi: https://doi.org/10.1101/264226
Lukas Meile
1Plant Pathology, Institute of Integrative Biology, ETH Zürich, Switzerland
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Daniel Croll
2Laboratory of Evolutionary Genetics, Institute of Biology, University of Neuchâtel, Switzerland
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  • ORCID record for Daniel Croll
Patrick C. Brunner
1Plant Pathology, Institute of Integrative Biology, ETH Zürich, Switzerland
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Clémence Plissonneau
1Plant Pathology, Institute of Integrative Biology, ETH Zürich, Switzerland
3UMR BIOGER, INRA, AgroParisTech, Université Paris-Saclay, Avenue Lucien Bretignières, BP 01, Thiverval-Grignon F-78850, France.
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Fanny E. Hartmann
4Ecologie Systématique Evolution, University Paris-Sud, AgroParisTech, CNRS, Université Paris-Saclay, Orsay, France
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Bruce A. McDonald
1Plant Pathology, Institute of Integrative Biology, ETH Zürich, Switzerland
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Andrea Sánchez-Vallet
1Plant Pathology, Institute of Integrative Biology, ETH Zürich, Switzerland
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  • For correspondence: andrea.sanchez@usys.ethz.ch
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Summary

  • Cultivar-strain specificity in the wheat-Zymoseptoria tritici pathosystem determines the infection outcome and is controlled by resistance genes on the host side, of which many have been identified. However, on the pathogen side, the molecular determinants of specificity are largely unknown.

  • We used genetic mapping, targeted gene disruption and allele swapping to characterize the recognition of the new avirulence factor Avr3D1. We then combined population genetic and comparative genomic analyses to estimate the evolutionary trajectory of Avr3D1.

  • Avr3D1 is specifically recognized by cultivars harboring the resistance gene Stb7 and triggers a strong defence response without preventing pathogen infection and reproduction. Avr3D1 resides in a cluster of putative effector genes located in a region populated by independent transposable element insertions. The gene is present in all 132 investigated strains and is highly polymorphic, with a total of 30 different protein variants. We demonstrated that certain amino acid mutations in Avr3D1 led to evasion of recognition.

  • These results demonstrate that quantitative resistance and gene-for-gene interactions are not mutually exclusive per se. Location of avirulence genes in highly plastic genomic regions likely facilitates accelerated evolution that enables escape from recognition by resistance proteins.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted February 23, 2018.
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A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch
Lukas Meile, Daniel Croll, Patrick C. Brunner, Clémence Plissonneau, Fanny E. Hartmann, Bruce A. McDonald, Andrea Sánchez-Vallet
bioRxiv 264226; doi: https://doi.org/10.1101/264226
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A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch
Lukas Meile, Daniel Croll, Patrick C. Brunner, Clémence Plissonneau, Fanny E. Hartmann, Bruce A. McDonald, Andrea Sánchez-Vallet
bioRxiv 264226; doi: https://doi.org/10.1101/264226

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