Genome-Wide Exon-Capture Approach Identifies Genetic Variants of Norway Spruce Genes Associated With Susceptibility to Heterobasidion parviporum Infection

Abstract

Root and butt rot caused by members of the Heterobasidion annosum species complex is the most economically important disease of conifer trees in boreal forests. Wood decay in the infected trees dramatically decreases their value and causes considerable losses to forest owners. Trees vary in their susceptibility to Heterobasidion infection, but the genetic determinants underlying the variation in the susceptibility are not well-understood. We performed the identification of Norway spruce genes associated with the resistance to Heterobasidion parviporum infection using genome-wide exon-capture approach. Sixty-four clonal Norway spruce lines were phenotyped, and their responses to H. parviporum inoculation were determined by lesion length measurements. Afterwards, the spruce lines were genotyped by targeted resequencing and identification of genetic variants (SNPs). Genome-wide association analysis identified 10 SNPs located within 8 genes as significantly associated with the larger necrotic lesions in response to H. parviporum inoculation. The genetic variants identified in our analysis are potential marker candidates for future screening programs aiming at the differentiation of disease-susceptible and resistant trees.

Low Water Availability Increases Necrosis in Picea abies after Artificial Inoculation with Fungal Root Rot Pathogens Heterobasidion parviporum and Heterobasidion annosum

“…A similar observation was made in an inoculation study of three-year-old Norway spruce ramets with H. parviporum [34]. However, this is in contrast to other studies, where Norway spruce saplings' height were negatively correlated with the necrosis length caused by H. parviporum [35]. Based on these results, saplings with lower values of growth parameters (in this case height) are not automatically considerably more sensitive to fungal inoculation, rather the necrosis development most likely involves multiple, interacting factors, e.g., different experimental settings and origins of pathogens and trees.…”

“…Gori et al [27] found that H. parviporum infection made P. abies more susceptible to drought stress at a low elevation site. The artificial fungal inoculation of seedlings and saplings of trees has been widely practiced under controlled greenhouse conditions, in order to investigate hosts susceptibility to Heterobasidion infection [34,35,47,48]. For the current experiment, three-year-old saplings were used instead of mature trees.…”

Evaluation of potential genetic and chemical markers for Scots pine tolerance against Heterobasidion annosum infection

“…In contrast, (Karlsson et al 2008) showed that stem diameter of P. abies had a strong negative correlation to both lesion size and fungal extension of H. parviporum. Another study revealed the diameter of Norway spruce saplings was significantly negatively correlated with lesion length particularly in xylem (Mukrimin et al 2018).…”

“…The inoculation method used ( Fig. 1) was similar as previously described (Keriö et al 2014;Mukrimin et al 2018). The stem surface was sterilized with 70% ethanol followed by making a hole with a 70% ethanol-sterilized puncher (10-mm diameter) through the tree bark to remove the rhytidome, phellem, and cambium.…”

Comprehensive Leaf Transcriptome of a Non-model Plant, Abelmoschus esculentus for the Functional Genomics Studies

“…In addition, sequence information from the transcriptome data can also be used to design exon capture arrays, to synthesize morpholino oligomers, to devise customized hybridization probes, to develop CRISPR/ Cas9 cascade for the investigation of gene function in association with disease condition or with other qualitative trait for plants with no genome sequence available. Mukrimin, et al [49] identified genetic variants of Norway spruce genes associated with susceptibility to Heterobasidion parviporum infection using exon capture approach. Sequence-specific morpholino oligomers are used to knock down gene mutation occurred during the diseased conditions [50].…”