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Genomic basis of white pine blister rust quantitative disease resistance and its relationship with qualitative resistance.

ABSTRACT: The genomic architecture and molecular mechanisms controlling variation in quantitative disease resistance loci are not well understood in plant species and have been barely studied in long-generation trees. Quantitative trait loci mapping and genome-wide association studies were combined to test a large single nucleotide polymorphism (SNP) set for association with quantitative and qualitative white pine blister rust resistance in sugar pine. In the absence of a chromosome-scale reference genome, a high-density consensus linkage map was generated to obtain locations for associated SNPs. Newly discovered associations for white pine blister rust quantitative disease resistance included 453 SNPs involved in wide biological functions, including genes associated with disease resistance and others involved in morphological and developmental processes. In addition, NBS-LRR pathogen recognition genes were found to be involved in quantitative disease resistance, suggesting these newly reported genes are qualitative genes with partial resistance, they are the result of defeated qualitative resistance due to avirulent races, or they have epistatic effects on qualitative disease resistance genes. This study is a step forward in our understanding of the complex genomic architecture of quantitative disease resistance in long-generation trees, and constitutes the first step towards marker-assisted disease resistance breeding in white pine species.

SUBMITTER: Weiss M

PROVIDER: S-EPMC10773528 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Genomic basis of white pine blister rust quantitative disease resistance and its relationship with qualitative resistance.

Weiss Matthew M Sniezko Richard A RA Puiu Daniela D Crepeau Marc W MW Stevens Kristian K Salzberg Steven L SL Langley Charles H CH Neale David B DB De La Torre Amanda R AR

The Plant journal : for cell and molecular biology 20200728 2

The genomic architecture and molecular mechanisms controlling variation in quantitative disease resistance loci are not well understood in plant species and have been barely studied in long-generation trees. Quantitative trait loci mapping and genome-wide association studies were combined to test a large single nucleotide polymorphism (SNP) set for association with quantitative and qualitative white pine blister rust resistance in sugar pine. In the absence of a chromosome-scale reference genome ...[more]

PMID: 32654344

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Project description:Since its introduction to North America in the early 1900s, white pine blister rust (WPBR) caused by the fungal pathogen Cronartium ribicola has resulted in substantial economic losses and ecological damage to native North American five-needle pine species. The high susceptibility and mortality of these species, including limber pine (Pinus flexilis), creates an urgent need for the development and deployment of resistant germplasm to support recovery of impacted populations. Extensive screening for genetic resistance to WPBR has been underway for decades in some species but has only started recently in limber pine using seed families collected from wild parental trees in the USA and Canada. This study was conducted to characterize Alberta limber pine seed families for WPBR resistance and to develop reliable molecular tools for marker-assisted selection (MAS). Open-pollinated seed families were evaluated for host reaction following controlled infection using C. ribicola basidiospores. Phenotypic segregation for presence/absence of stem symptoms was observed in four seed families. The segregation ratios of these families were consistent with expression of major gene resistance (MGR) controlled by a dominant R locus. Based on linkage disequilibrium (LD)-based association mapping used to detect single nucleotide polymorphism (SNP) markers associated with MGR against C. ribicola, MGR in these seed families appears to be controlled by Cr4 or other R genes in very close proximity to Cr4. These associated SNPs were located in genes involved in multiple molecular mechanisms potentially underlying limber pine MGR to C. ribicola, including NBS-LRR genes for recognition of C. ribicola effectors, signaling components, and a large set of defense-responsive genes with potential functions in plant effector-triggered immunity (ETI). Interactions of associated loci were identified for MGR selection in trees with complex genetic backgrounds. SNPs with tight Cr4-linkage were further converted to TaqMan assays to confirm their effectiveness as MAS tools. This work demonstrates the successful translation and deployment of molecular genetic knowledge into specific MAS tools that can be easily applied in a selection or breeding program to efficiently screen MGR against WPBR in Alberta limber pine populations.

Project description:BackgroundThe fungus Cronartium ribicola (Cri) is an economically and ecologically important forest pathogen that causes white pine blister rust (WPBR) disease on five-needle pines. To cause stem cankers and kill white pine trees the fungus elaborates a life cycle with five stages of spore development on five-needle pines and the alternate host Ribes plants. To increase our understanding of molecular WP-BR interactions, here we report genome-wide transcriptional profile analysis of C. ribicola using RNA-seq.ResultscDNA libraries were constructed from aeciospore, urediniospore, and western white pine (Pinus monticola) tissues post Cri infection. Over 200 million RNA-seq 100-bp paired-end (PE) reads from rust fungal spores were de novo assembled and a reference transcriptome was generated with 17,880 transcripts that were expressed from 13,629 unigenes. A total of 734 unique proteins were predicted as a part of the Cri secretome from complete open reading frames (ORFs), and 41 % of them were Cronartium-specific. This study further identified a repertoire of candidate effectors and other pathogenicity determinants. Differentially expressed genes (DEGs) were identified to gain an understanding of molecular events important during the WPBR fungus life cycle by comparing Cri transcriptomes at different infection stages. Large-scale changes of in planta gene expression profiles were observed, revealing that multiple fungal biosynthetic pathways were enhanced during mycelium growth inside infected pine stem tissues. Conversely, many fungal genes that were up-regulated at the urediniospore stage appeared to be signalling components and transporters. The secreted fungal protein genes that were up-regulated in pine needle tissues during early infection were primarily associated with cell wall modifications, possibly to mask the rust pathogen from plant defenses.ConclusionThis comprehensive transcriptome profiling substantially improves our current understanding of molecular WP-BR interactions. The repertoire of candidate effectors and other putative pathogenicity determinants identified here are valuable for future functional analysis of Cri virulence and pathogenicity.

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Genomic basis of white pine blister rust quantitative disease resistance and its relationship with qualitative resistance.

Publications

Genomic basis of white pine blister rust quantitative disease resistance and its relationship with qualitative resistance.

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