Association genetics identifies a specifically regulated Norway spruce laccase gene, PaLAC5, linked to Heterobasidion parviporum resistance

Abstract

It is important to improve the understanding of the interactions between the trees and pathogens and integrate this knowledge about disease resistance into tree breeding programs. The conifer Norway spruce (Picea abies) is an important species for the forest industry in Europe. Its major pathogen is Heterobasidion parviporum, causing stem and root rot.In this study, we identified 11 Norway spruce QTLs (Quantitative trait loci) that correlate with variation in resistance to H. parviporum in a population of 466 trees by association genetics. Individual QTLs explained between 2.1 and 5.2% of the phenotypic variance. The expression of candidate genes associated with the QTLs was analysed in silico and in response to H. parviporum hypothesizing that (a) candidate genes linked to control of fungal sapwood growth are more commonly expressed in sapwood, and; (b) candidate genes associated with induced defences are respond to H. parviporum inoculation. The Norway spruce laccase PaLAC5 associated with control of lesion length development is likely to be involved in the induced defences. Expression analyses showed that PaLAC5 responds specifically and strongly in close proximity to the H. parviporum inoculation. Thus, PaLAC5 may be associated with the lignosuberized boundary zone formation in bark adjacent to the inoculation site.

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

“…Recent genomic and molecular methods employed in model and crop species have allowed a good understanding of the genes, gene families, and pathways involved in these processes (Nelson et al ., 2018). Most of this knowledge, however, comes from the study of large‐effect qualitative disease resistance loci involved in pathogen recognition, while our understanding of the molecular mechanisms controlling variation in small‐effect quantitative disease resistance loci is still limited in plant species and almost non‐existent in long‐generation trees (Poland et al ., 2009; Neale and Kremer, 2011; Kovalchuk et al ., 2013; Corwin and Kliebenstein, 2017; Elfstrand et al ., 2020). Greater attention to the study of disease responses is warranted in long‐generation tree species as theoretical work suggests long‐lived plants may (i) have higher levels of polymorphism and rates of evolution of disease resistance than short‐lived plants (Bruns et al ., 2015), (ii) be more reliant on systemic‐induced resistance to respond to pathogens (Bonello et al ., 2006), and (iii) have experienced expansions in important gene families related to defense (Hamberger et al ., 2011; Porth et al ., 2011; Warren et al ., 2015; De La Torre et al ., 2020).…”

Combining transcriptomics and genetic linkage based information to identify candidate genes associated with Heterobasidion-resistance in Norway spruce

“…The approach in this study allowed us to work with well-studied plant materials and to use a narrow genetic base to generate initial data 41 , 42 and identify potential resistance candidates for further work, which was one of the primary objectives of this study. Clearly we missed out on potential candidate genes which are not associated with the QTL regions in the genetic linkage map and also candidates associated with QTLs which are not present in the original study 43 , 44 . Nevertheless, combining genomic and transcriptomic analysis we identified 124 candidate resistance genes which could be considered as candidates for induced resistance.…”

Killing two enemies with one stone? Genomics of resistance to two sympatric pathogens in Norway spruce

“…It is possible that genetic variation in the region linked to this QTL drives the positive pleiotropic effect we observe and could therefore be an example of multiple disease resistance conferred by individual genes clustered in the genome. Similarly, a SNP in PaLAC5 with a synergistic pleiotropic effect on LL to both pathogens (Figure 3, lower‐left quadrant), encodes a stress induced laccase (Koutaniemi et al, 2015; Laitinen et al, 2017) which is associated with resistance to H. parviporum (Elfstrand et al 2020). This gene is specifically and differentially expressed in tissues after infection by H. parviporum , and is likely to be involved in the formation of the ligno‐suberized boundary zone (Elfstrand et al 2020).…”

“…Similarly, a SNP in PaLAC5 with a synergistic pleiotropic effect on LL to both pathogens (Figure 3, lower‐left quadrant), encodes a stress induced laccase (Koutaniemi et al, 2015; Laitinen et al, 2017) which is associated with resistance to H. parviporum (Elfstrand et al 2020). This gene is specifically and differentially expressed in tissues after infection by H. parviporum , and is likely to be involved in the formation of the ligno‐suberized boundary zone (Elfstrand et al 2020). Ligno‐suberized boundary zone formation is a common feature of angiosperm and gymnosperm trees in response to a wide range of pathogens (Pearce, 1996; Woodward, 1992), which is in line with the synergistic pleiotropic effect observed in PaLAC5 .…”