PLANT PATHOLOGY | AGRICULTURE
Plant Immunity: Qualitative and Quantitative Resistance
Plant immunity consists of dual resistance mechanisms that are qualitative and quantitative in nature.
Phytopathogens impair the normal physiology of their host plants. Microbes feed on plants for growth energy and multiplication. Basically, there are three modes by which pathogens derive nutrients from their host plants to fulfill their energy requirements.
Biothrophs feed off the living host tissues of the host while the necrotrophs obtain energy from the dead host cells and tissues. The other microbes live between biotrophs and necrotrophs. First, they feed on living cells and later turned to be the feeders of dead host cells and tissues.
To combat or keep them away from themselves, plants play as killers. They intelligently use their cellular machinery to fight back through their immune responses. Immunity depends on the perception, signal transduction, and the defense response. Plant perception of any damage or microbe-associated molecular patterns by cell surface receptors initiates a cascade of signaling responses. Signaling cascade consists of reactive oxygen species (ROS, production of growth, and defense-related hormones that specifies the expression of various genes to kill the pathogens. Plant resistance to such virulent factors come in dual nature: qualitative resistance and quantitative resistance.
Resistance to pathogens is a prerequisite to food security and safety. In plants resistance to pathogens is controlled by two mechanisms the monogenic or qualitative and polygenic or quantitative. The qualitative mechanism confers two phenotypic responses either complete resistance to specific pathogen infection or susceptibility to that pathogen. The qualitative resistance shows an R–gene interaction with a specific pathogen gene. In this mechanism, the resistance reaction involves the recognition of virulent factors, then mediates the resistance reaction known as the hypersensitive response (HR).
The qualitative R genes with major resistance effect block the pathogen at the infection site and ultimately prevents the pathogen from further spread into the host cell. This mechanism expresses two discrete traits — either the host plant is resistant or susceptible. In qualitative resistance, only a single gene is involved with a major trait of susceptibility or resistance. While in quantitative resistance more than one gene is involved with both major and minor effects. Quantitative resistance is a broader term in plant-pathogen interactions but the more general definition is: it is polygenic resistance with partial effect. It does not block the pathogen at the infection site but decreases the symptom severity, pathogen colonization & multiplication.
According to (Niks et al., 2015) sometimes the quantitative resistance confers complete resistance to certain pathogens with the combination of resistant QTL (quantitative trait loci). For example in tomato, the combination of strong quantitative trait loci rx1, rx2, and rx3 produces complete resistance to Xanthomonas campestris. Quantitative trait loci is a genomic region on a chromosome that is associated with a particular phenotypic trait. And these quantitative traits are phenotypic traits linked with more than one gene. These genes produce strong and weak resistance effects relying on these quantitative traits.
The field resistance or quantitative resistance can be better assessed in adult plants and it is durably effective against all races of pathogens even under disease favoring environmental conditions. It has a partial effect with a constant expression of resistance to susceptibility at various stages during plant growth and development. The genes that are involved in quantitative resistance responses are the allelic variants of defense genes. The allelic variation of such genes leads to varying expression levels under various growth conditions in the plant's life. These variant defense genes show higher quantitative resistance response due to higher expression rates and made it difficult for pathogen effectors to manipulate plant cells. Effectors are pathogen molecules that are released into plant cell cytoplasm to remodel plant defense responses. These molecules bind only to certain host cell proteins to suppress the defense responses.
Niks and Marcel proposed the mechanism by which effectors target their plant cell factors. They hypothesized that interaction between effector and plant targets depends on the successful recognition or lack of recognition of target motifs, regions, and products. The molecular mechanism of interaction alters the gene expression, products, gene function, and structure. The alterations in the structure of plant targets prevent the binding of effector molecules — this variation in plant targets is significant in quantitative resistance (QR). These genes are the relevant candidate genes that contribute to QR.
Quantitative resistance (QR) is durably effective than qualitative resistance. Qualitative resistance is effective against a particular pathogen race while quantitative resistance is broad-spectrum and efficient even under disease favourable environment. The genes underlying quantitative resistance is not well studied. The determination of major combinations of QTLs in main crops (wheat, rice, and maize) will enhance their efficacy against disease and food security. Due to its durability and broader nature, quantitative resistance is a promising tool in plant breeding programs through marker-assisted breeding.
