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Proc Natl Acad Sci U S A. 2018 Nov 6;115(45):11573-11578. doi: 10.1073/pnas.1804428115. Epub 2018 Oct 18.

Association mapping, transcriptomics, and transient expression identify candidate genes mediating plant-pathogen interactions in a tree.

Author information

1
Biosciences Division, Oak Ridge National Laboratory, Oak Ridge, TN 37831.
2
Department of Botany and Plant Pathology, Oregon State University, Corvallis, OR 97331.
3
Complex Carbohydrate Research Center, University of Georgia, Athens, GA 30602.
4
Joint Genome Institute, US Department of Energy, Walnut Creek, CA 94598.
5
Department of Plant Pathology, North Dakota State University, Fargo, ND 58102.
6
HudsonAlpha Institute for Biotechnology, Huntsville, AL 35806.
7
Department of Botany and Plant Pathology, Oregon State University, Corvallis, OR 97331; jared.leboldus@science.oregonstate.edu.
8
Forest Engineering, Resources, and Management, Oregon State University, Corvallis, OR 97331.

Abstract

Invasive microbes causing diseases such as sudden oak death negatively affect ecosystems and economies around the world. The deployment of resistant genotypes for combating introduced diseases typically relies on breeding programs that can take decades to complete. To demonstrate how this process can be accelerated, we employed a genome-wide association mapping of ca 1,000 resequenced Populus trichocarpa trees individually challenged with Sphaerulina musiva, an invasive fungal pathogen. Among significant associations, three loci associated with resistance were identified and predicted to encode one putative membrane-bound L-type receptor-like kinase and two receptor-like proteins. A susceptibility-associated locus was predicted to encode a putative G-type D-mannose-binding receptor-like kinase. Multiple lines of evidence, including allele analysis, transcriptomics, binding assays, and overexpression, support the hypothesized function of these candidate genes in the P. trichocarpa response to S. musiva.

KEYWORDS:

Populus trichocarpa; association mapping; disease resistance; invasive disease; septoria canker

PMID:
30337484
PMCID:
PMC6233113
DOI:
10.1073/pnas.1804428115
[Indexed for MEDLINE]
Free PMC Article

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