Plant resistance to pathogens as a result of gene interaction

Modern information on the genomics of plants and plants’ pathogens as well the achievements of molecular biology have made it possible to state the participation of gene products, proteins, in the organization of molecular complexes that are assembled to implement a certain character of the phenotype. The character of plant “resistance/sensitivity” to a certain biotic factor is also interesting because there is an interaction not only between the genes of one organism, but between the genes of organisms that lie in different kingdoms of life.Plant resistance to pathogens can be passive (provided mainly by characters of plant morphology) and active. Active resistance is formed as a result of the penetration of the pathogen or its elicitors and effectors into the plant. Active protection of the plant at the molecular level is expressed in the launch of the MAPK cascade, the accumulation of reactive oxygen species, and an increase in the flow of calcium ions to the cell. Active protection can be implemented on two levels. The first level, RTI (PAMP Triggered Immunity), develops in response to plant contact with a wide range of non-adapted pathogens. The resistance (immunity) that is formed in this case is called non-specific, or horizontal, or quantitative. The molecular instrument for initiating the defensive reaction is the PRR (Pattern Recognition Receptors). Adapted pathogens are able to overcome RTI by sending effectors to plant cells. These are protein molecules whose function is to create conditions within the cell that are more permissive to the pathogen. The effector can be recognized by the plant’s specific NLR (Nod-Like Receptors), and complementation occurs between the two. There are other specific plant molecules, nonNLR, with a different type of protein product interaction for recognition. In both cases, the second level of protection, ETI (Effector Triggered Immunity), develops. The set of molecular processes that occur at the second level of protection does not differ from the set of the first level, but the processes occur more intensively and are accompanied by the death of the affected cells. This prevents the further spread of the pathogen throughout the plant. The molecular events of the first and second levels of protection are not isolated. The interaction between them involving the products of plant genes and pathogen genes is described by the “zig-zag-zig”-model, invasion model, and the integrated iceberg model. The interaction of plant genes for effector recognition is described by the “guard” and “decoy” models. To initiate a defensive reaction, plant receptors, which can sometimes differentiate into sensors and helpers, form protein complexes, resistosomes.