Plant resistance against disease can be provided by a single gene of large effect or by multiple genes and each conferring incomplete resistance. When expression and the inheritance of the trait is under control of many genes it is called quantitative resistance. The complexity of these traits come from underlying genes/loci as well as from the multitude potential allelic interactions within and between the genes involved (Yuan et al., 2023).
Quantitative disease resistance is expressed as a continuous trait and can be influenced by additive, dominance and epistasis gene action. Additive effect arises from the independent contribution of individual alleles, while dominance refers to interaction between allele at the same locus and epistatsis involves interactions between alleles at different loci. Epistasis occurs in following way (Miko 2008):
- When two or more loci interact to create new phenotypes
- Whenever an allele at one locus masks the effects of alleles at one or more loci
- Whenever an allele at one locus modifies the effects of alleles at one or more other loci
Different disease resistance specificities often map to tightly linked regions of plant genomes, referred to as complex loci (Ellis and Jones 2003). Quantitative trait loci (QTL) analysis shows genetic architecture of resistance to diseases and is characterized by different modes of gene action (Hudson et al., 2025). These modes of gene action contribute to the quantitative disease resistance and can affect the level of heterosis or hybrid vigor, observed in resistant variety. Heterosis or the hybrid vigor is the improved performance of a hybrid compared with its parents, which is caused by the nonadditive gene action and is fundamental to breeding of several crops (Hudson et al., 2025). The heterosis for resistance appears to be dependent on both hybrid genotype and disease. Locus expansion and contraction may occur by unequal crossing over events at meiosis. Resistance genes can also occur in simple loci containing only a single gene. Multiple resistance specificities can be encoded by different allelic variants of a single gene (Ellis and Jones 2003). Upon comparison between closely related resistance (R) genes from a single locus, it is evident that variation is generated by standard evolutionary processes, including point mutation, deletion, insertion and meiotic recombination (Ellis and Jones 2003). Discovery of R genes and R gene loci provides an insight into R genes function and evolution and leads to novel strategies for disease control (Hammond-Kosack and Jones 1997). Single nucleotide polymorphisms at R-gene and pattern recognition receptor loci can introduce quantitative differences in resistance phenotype (Roux et al., 2014). The two R (Xa4 and Xa21) genes showed complete dominance against the avirulent Xanthomonas oryzae pv. oryzae racesand had large residual effects against virulent ones (Li et al., 2001). They acted independently and cumulatively, suggesting their involvement in different pathway of the rice defensive system (Li et al., 2001). Resistance to zonate leaf spot disease in forage sorghum revealed overdominance (Grewal 1988).
Additive, Dominance and Epistasis Gene Action:
Inheritance of resistance to the disease is controlled by both additive and non-additive gene action. The term additive and non-additive can be confusing because their meaning depends on whether the scope of inference is a single locus or multiple loci (Holland 2001). Additive gene action in reference to a single locus implies the lack of dominant gene action. Additive gene action in reference to two or more loci refers to the lack of epistasis (Holland 2001). The effect of a gene is said to be additive when each additional gene enhances the expression of the trait by equal increments (Author anonymous and year is not mentioned). Additive effect apply to the allelic interaction at the same locus. The performance of an allele is the same irrespective of other allele at the same locus (Author anonymous and year is not mentioned). Non-additive genetic effect is any deviation from this additive effect example dominance and epistasis. Earliness and powdery mildew resistance showed a large epistatic variance (Goldringer et al., 1997). Race non-specific resistance also known as “adult plant resistance” (APR) to wheat rust is conferred by multiple additive genes (Li et al., 2016). Some APR genes are both durable and broad-spectrum, individual APR gene don’t confer agronomically acceptable levels of disease-resistance, but a distinct solution is to combine multiple ASR (all plant developmental stage resistance) genes and/or multiple additive APR genes (Ayliffe et al., 2022).
Dominance variance has two components such as variance due to homozygous alleles (which is additive) and variance due to heterozygous genotypic values. Dominance effects are deviation from additivity that make heterozygote resemble one parent more than the other and when dominance is complete the heterozygote is equal to the homozygote in effect (allele i.e. Aa=AA) (Author anonymous and year is not mentioned). Additive and additive by dominance gene effect was the only form of gene effects involved in the inheritance of resistance to the disease (Kufor 2016). On the contrary Nalugo et al.(2013) found the interaction of dominance x dominance with duplicate epistatic effect on the resistance to groundnut rosette disease. This contradiction may be due to the difference in the parent genotypes used (Kufor 2016). The inheritance of rust resistance in groundnut is conditioned by dominance gene action, while kernel yield was controlled by additive gene action (Daudi et al., 2021). Epistasis can make substantial contribution to the additive, dominance and interaction genetic variances (Cheverud and Routman 1995). Host plant resistance is a disease management strategy.
References:
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BIOLOGICAL PROCESSES- A NATURE'S GIFT 