Disease resistance is a heritable trait in plants. Genetic (heritable) resistance variation in plants is of two main forms the qualitative and the quantitative resistance. The qualitative resistance or gene for gene resistance prevents infection by pathogen in a strain-specific manner and where response to pathogen is inherited as discrete variation at a small number of genes. While the quantitative resistance reduces the progress of infection but not absence of disease and are inherited as a continuous variation through combined effect of several genes (Hood et al., 2023). Both form of resistance may occur in the same host-pathogen system or co-occur with in the same host population (Ericson and Burdon 2009; Laine et al 2011). Quantitative variation may modulate the qualitative gene-for-gene responses like hypersensitive response (HR) leading to cell death (Penning et al., 2004).
Quantitative resistance is generally more durable than the qualitative resistance and has the potential to preserve major-gene effects (Parlevliet 2002; Pilet-Nayel et al., 2017). Combining quantitative resistance with major resistance (R) gene has proven to be an approach for extending the effectiveness of major genes. In plant genomics, improved tools and methods are becoming available to integrate quantitative resistance into breeding strategies (Pilet-Nayel et al., 2017). Qualitative disease resistance is involved in plant defense response against biotrophic pathogens (Zhang et al., 2013). Studies on necrotrophic and hemibiotrophic pathogen suggest that resistance require concerted action of multiple genes with minor effect, which is the nature of quantitative disease resistance (Zhang et al., 2013; Gou et al., 2022). The plant resistance to pathogen attack is expressed as reduced susceptibility ranging from high susceptibility to HR the shades of gray (Kushalappa et al., 2016). The resistant genes (alleles) interact in a gene-for-gene way with a virulence gene (alleles) in the pathogen to give an incompatible reaction (Parlevliet 2002).
The plant receptors localized at plasma membrane are receptor-like kinases (RLKs), which at C-terminal end bind to elicitors in the apoplast and at N-terminal bind to kinases in the cytosol or receptor-like proteins (RLPs) which have no intracellular kinase domain (Macho and Zipfel 2015; Kushalappa et al., 2016). Following invasion pathogen produce elicitors [pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs)] which is recognized by the plant elicitor recognition receptors [ELRRs produced by RELRR genes, former: pattern recognition receptor (PRR)], while the specialized pathogens produce effectors which are recognized by effector recognition receptors (ERR by RERR genes; former: receptor proteins by R genes). Upon recognition of elicitors the RELRR genes induce elicitor-triggered immunity (ELTI Former: PTI) while recognition of effectors the RERR genes induce effector-triggered immunity (ETI). A weak or absence of ELTI or ETI or non-functionality of genes involved, and suppression by other elicitors such as enzymes and toxins enable pathogen to advance which then is suppressed by resistance-related metabolites (RRMs) such as callose, phytoanticipins and phytoalexins and resistance-related proteins (RRPs) such as pathogenesis-related proteins (Jones and Dangl 2006; Kushalappa et al., 2016). The HR is also controlled by many genes that produces different RRMs and RRPs and so is the quantitative resistance. The resistance thus depends on the type and amount of RRMs and RRPs produced which in turn depends on hierarchies of R genes (Kushalappa et al., 2016).
Loci controlling quantitative resistance contain few same causal genes that mediate qualitative resistance, but the mechanism of quantitative resistance extends beyond pathogen recognition (Corwin and Kliebenstein 2017). Most causal genes for quantitative resistance encode specific defense-related response such as strengthening of cell wall or biosynthesis of defense compounds (Corwin and Kliebenstein 2017). Many quantitative disease resistance gene based on biological function are classified into several functional categories such as pathogen perception, signal transduction, phytohormone homeostasis, metabolite biosynthesis and transport as well as epigenetic regulation (Gou et al., 2022). Quantitative resistance to various fungal, bacterial and nematode pathogens causing disease, provide an insight into number of quantitative resistance loci, interaction between pathogen biology, plant development and biochemistry and the relationship between qualitative and quantitative loci (Young 1996). Langlands-Perry et al.(2023) hypothesize that genes involved in quantitative and qualitative plant-pathogen interactions are similar. Quantitative trait loci (QTL) are genetic regions linked to specific phenotypic traits, which are shaped by both genetic and environmental factors (Ofori et al., 2025). These loci can be found on various chromosomes and are frequently used to identify potential gene responsible for particular trait. The disease resistance gene which include the R gene, defense-regulator genes and QTL provide resistance against pathogens were identified and mapped (Liu et al., 2021; Ofori et al., 2025). QTL: a locus with an effect on quantitative trait (i.e. a trait showing continuous variation) (Poland et al., 2008).
Identification of QTLs controlling agricultural traits is vital. The QTL mapping help in identifying region of the genome that are associated with plant disease resistance. Many QTL have been detected in rice including those for disease and insect resistance, yield and grain quality, salt, drought, submergence tolerance and nutrient utilization efficiency (Hao and Lin 2010). QTL can be specific (i.e. detected with only one isolate) or non-specific (i.e. broad-spectrum) (Pilet-Nayel et al., 2017) to a pathogen species, while some multiple disease resistance QTL confer resistance to multiple pathogens with diverse lifestyle (biotrophic, hemibiotrophic and necrotrophic) (Ellis et al., 2014; Wiesner-Hanks and Nelson 2016). The resistance at the chromosomal level may be by clusters of tightly linked genes or by individual genes with pleiotropic effects (Wiesner-Hanks and Nelson 2016). Plant must detect and respond to the different pathogenic strategies.
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