Disease has major impact on plant population. Plants deploy mechanisms to resist pathogens with diverse pathogenic strategies. Genetic variation for disease resistance is characteristic of all species and that this variation may have profound consequence for patterns of disease incidence and prevalence (Laine and Tellier 2008). Virulent pathogens occur more frequently in highly resistant host, while avirulent pathogens dominated susceptible population (Thrall and Burdon 2003). The genotype-genotype interaction at genetic level determines the outcome and severity of disease. The interacting gene does not reveal which host genotype(s) is/are resistant to which pathogen genotype(s) (Markle et al., 2024).
Plants have two different resistance strategies which are qualitative resistance and quantitative resistance based on distinct phenotypic outcomes and inheritance modes (Niks et al., 2015). Quantitative disease resistance refers to incomplete or reduced level of resistance which is usually controlled by multiple quantitative trait loci (QTL) of minor to moderate effect (Niks et al., 2015; Corwin and Kliebenstein 2017; Gou et al., 2022). The several genes controlling quantitative resistance are associated with genomic regions or QTL, contributing each with variable effect, to the phenotype of resistance to a pathogen. Quantitative resistance does not block but only reduces pathogen multiplication, plant colonization and symptom severity or can delay the development of pathogen strains (Susi and Laine 2015; Pilet-Nayel et al., 2017). While the qualitative resistance is defined as the number of pathogen strains that the plant can resist (Susi and Laine 2015).
However, a combination of resistance QTL can lead to total resistance in some cases i.e. when QTL have strong effect (Niks et al., 2015; Pilet-Nayel et al., 2017). Whereas qualitative resistance is either complete or a high level of resistance which is based on the effect of single gene that segregate in a population, a bimodal distribution of disease resistance is observed (Pilet-Nayel et al., 2017; Gou et al., 2022). There are various terms used to refer quantitative resistance such as field resistance, adult plant resistance and basal resistance, reflect the several properties attributed to it (Niks et al., 2015). Accordingly, Niks et al.(2015) indicated two distinct aspect of quantitative and qualitative resistance, one aspect is phenotypic phenomenon that the quantitative resistance is incomplete, i.e. allowing some reproduction by the pathogen hence some epidemic progress or qualitative i.e. resistance that completely impedes reproduction of pathogen. The second aspect to which the term quantitative and qualitative may refer is the mode of inheritance (Niks et al., 2015). On considering mode of inheritance, the quantitative refers to a resistance that is based on several gene, contributing to reduced level of resistance (Niks et al., 2015). This concept is applied by the term polygenic resistance. When authors refer quantitative resistance as basal resistance, they assume resistance is due to incomplete effector-triggered susceptibility (incompletely suppressed pattern triggered immunity) rather than based on constitutive defense components (Niks et al., 2015).
Studies on the detection of pathogens have focused on microbe- or pathogen-associated molecular patterns (MAMPs/PAMPs) signals found as a part of large effect gene-for-gene resistance pathosystem (Corwin and Kliebenstein 2017). PAMPs perception evolve quantitatively in Arabidopsis and among close relatives, which contrast with the changes in recognition associated with the evolution of resistance (R) gene (Vetter et al., 2012). The hypothesis that quantitative resistance to biotrophic filamentous plant pathogen is a basal resistance i.e. poor suppression of PAMP-triggered immunity by effectors (Niks et al., 2015).Infection and resistance are strain specific. Variation in the virulence of pathogen lines may affect colonization by the pathogen (Laine 2004). As the quantitative disease resistance is controlled by several QTL and is influenced by environmental conditions, it is more challenging to identify and then exploit the underlying genes, as compared to qualitative resistance (Gou et al., 2022).
Past studies have focused on examples of qualitative resistance, where the underlying genetic architecture relies on a few gene of large effect while the genetic architecture underlying quantitative resistance may involve many genes with small to moderate effects (Corwin and Kliebenstein 2017). The QTL involved in polygenic induced resistance has both epistatic and additive effect (Lefebvre and Palloix 1996; Manzanares-Dauleux et al., 2000; Calenge et al., 2005). Each gene locus has an independent effect on a single phenotype. When two different genes (digenic) contribute to a single phenotype, and their effects are not merely additive those gene are said to be epistatic. Epistasis occur in a variety of different ways and result in variety of different phenotypic ratio. Epistasis occurs in following scenario (Miko 2008):
- whenever two or more loci interact to create new phenotype
- when an allele at one locus masks the effect of alleles at one or more other loci
- when an allele at one locus modifies the effect of alleles at one or more other loci
Langlands-Perry et al.(2023) hypothesize that genes involved in quantitative and qualitative plant-pathogen interactions are similar. Plants qualitative resistance is based on R gene which are responsible for pathogen recognition and induction of defense responses whereas quantitative resistance is to be under polygenic control (Bergelson et al., 2001; Poland et al., 2009). Qualitative resistance often induces hypersensitive response (HR) leading to programmed cell death near the infection site controlling the pathogen growth (Jones and Dangl 2006; Stotz et al., 2014). While the remainder of the reduced susceptibility is quantitative resistance (Kushalappa et al., 2016). QTL and R-genes can maintain the effectiveness of plant resistance to pathogen attacks.
References:
Bergelson, J., Kreitman, M., Stahl, E. A. and Tian, D. 2001 Evolutionary Dynamics of Plant R-Genes. Science 292(5525): 2281
doi: 10.1126/science.1061337
Calenge, F., Drouet, D., Denance, C., Van de Weg, W. E., Brisset, M-N., Paulin, J-P. and Durel, C-E. 2005 Identification of a Major QTL Together with Several Minor Additive or Epistatic QTLs for Resistance to Fire Blight in Apple in Two Related Progenies. Theor. Appl. Genet. 111(1): 128 – 135
doi: 10.1007/s00122-005-2002-z
Corwin, J. A. and Kliebenstein, D. J. 2017 Quantitative Resistance: More than Just Perception of a Pathogen. Plant Cell 29(4): 655 – 665
doi: 10.1105/tpc.16.00915
Gou, M., Balint-Kurti, P., Xu, M. and Yang, Q. 2022 Quantitative Disease Resistance: Multifaceted Players in Plant Defense. JIPB 65(2): 594 -610
doi.org/10.1111/jipb.13419
Jones, J. D. G. and Dangl, J. L. 2006 The Plant Immune System. Nature 444(7117): 323 – 329
doi: 10.1038/nature05286
Kushalappa, A. C., Yogendra, K. N. and Karre, S. 2016 Plant Innate Immune Response: Qualitative and Quantitative Resistance. Critical Reviews in Plant Sciences 35(1): 38 – 55
doi.org/10.1080/07352689.2016.1148980
Laine, A-L. 2004 Resistance Variation within and Among Host Populations in a Plant-Pathogen Metapopulation: Implications for Regional Pathogen Dynamics. J. Ecol. 92(6): 990 – 1000
doi.org/10.1111/j.0022-0477.2004.00925.x
Laine, A-L. and Tellier, A. 2008 Heterogeneous Selection Promotes Maintenance of Polymorphism in Host-Parasite Interactions. Oikos 117: 1281 -1288
doi: 10.1111/j.2008.0030-1299.16563.x
Langlands-Perry, C., Pitarch, A., Lapalu, N., Cuenin, M., Bergez, C., Noly, A., Amezrou, R., Gelisse, S., Barrachina, C., Parrinello, H., Suffert, F., Valade, R. and Marcel, T. C. 2023 Quantitative and Qualitative Plant-Pathogen Interactions Call Upon Similar Pathogenicity Genes with a Spectrum of Effects. Front. Plant Sci. 14: 1128546
doi: 10.3389/fpls.2023.1128546
Lefebvre, V. and Palloix, A. 1996 Both Epistatic and Additive Effects of QTLs are Involved in Polygenic Induced Resistance to Disease: A Case Study, the Interaction Pepper-Phytophthora capsica Leonian. Theor. Appl. Genet. 93(4): 503 – 511
doi: 10.1007/BF00417941
Manzanares-Dauleux, M. J., Delourme, R., Baron, F. and Thomas, G. 2000 Mapping of One Major Gene and of QTLs Involved in Resistance to Clubroot in Brassica napus. Theor. Appl. Genet. 101(5): 885 – 891
doi: 10.1007/s001220051557
Markle, H., John, S., Metzger, L., Consortium, S-H., Ansari, M. A., Pedergnana, V. and Tellier, A. 2024 Inference of Host-Pathogen Interaction Matrices from Genome-Wide Polymorphism Data. Mol. Biol. Evol. 41(9): msae176
doi.org/10.1093/molbev/msae176
Miko, I. 2008 Epistasis: Gene Interaction and Phenotype Effects. Nature Education 1(1): 197
Niks, R. E., Qi, X. and Marcel, T. C. 2015 Quantitative Resistance to Biotrophic Filamentous Plant Pathogens: Concepts, Misconceptions and Mechanisms. Annu. Rev. Phytopathol. 53: 445 – 470
doi: 10.1146/annurev-phyto-080614-115928
Pilet-Nayel, M-L., Moury, B., Caffier, V., Montarry, J., Kerlan, M-C., Fournet, S., Durel, C-E. and Delourme, R. 2017 Quantitative Resistance to Plant Pathogens in Pyramiding Strategies for Durable Crop Protection. Front. Plant. Sci. 8: 1838
doi: 10.3389/fpls.2017.01838
Poland, J. A., Balint-Kurti, P. J., Wisser, R. J., Pratt, R. C. and Nelson, R. J. 2009 Shades of Gray: The World of Quantitative Disease Resistance. Trends Plant Sci. 14(1): 21 – 29
doi: 10.1016/j.tplants.2008.10.006
Stotz, H. U., Mitrousia, G. K., de Wit, P. J. G. M. and Fitt, B. D. L. 2014 Effector-triggered Defense against Apoplastic Fungal Pathogens. Trends Plant Sci. 19(8): 491 – 500
doi: 10.1016/j.tplants.2014.04.009
Susi, H. and Laine, A-L. 2015 The Effectiveness and Costs of Pathogen Resistance Strategies in a Perennial Plant. J. Ecol. 103(2): 303 – 315
doi.org/10.1111/1365-2745.12373
Thrall, P. H. and Burdon, J. J. 2003 Evolution of Virulence in a Plant Host-Pathogen Metapopulation. Science 299(5613): 1735 – 1737
doi: 10.1126/science.1080070
Vetter, M. M., Kronholm, I., He, F., Haweker, H., Reymond, M., Bergelson, J., Robatzek, S. and de Meaux, J. 2012 Flagellin Perception Varies Quantitatively in Arabidopsis thaliana and its Relatives. Mol. Biol. Evol. 29(6): 1655 – 1667
doi: 10.1093/molbev/mss011
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