Hypersensitive response
HR is characterized by the rapid death of cells in the local region surrounding an infection and it serves to restrict the growth and spread of pathogens to other parts of the plant.
[2] HR is commonly thought of as an effective defence strategy against biotrophic plant pathogens, which require living tissue to gain nutrients.
The situation becomes complicated when considering pathogens such as Phytophthora infestans which at the initial stages of the infection act as biotrophs but later switch to a necrotrophic lifestyle.
When a pathogen is sensed, the ADP is exchanged for Adenosine triphosphate (ATP) and this induces a conformational change in the NLR protein, which results in HR.
The C-terminus of the NLRs consists of a leucine-rich repeat (LRR) motif, which is involved in sensing the pathogen virulence factors.
Reactive oxygen species also trigger the deposition of lignin and callose, as well as the cross-linking of pre-formed hydroxyproline-rich glycoproteins such as P33 to the wall matrix via the tyrosine in the PPPPY motif.
[10] Activation of HR also results in disruption of the cytoskeleton, mitochondrial function and metabolic changes, all of which might be implicated in causing cell death.
An example of this can be observed in plant resistance to the rice blast pathogen, where the RGA5 NLR has a heavy-metal-associated (HMA) domain integrated into its structure, which is targeted by multiple effector proteins.
When the resistosome is assembled, a helix sticks out from the N-terminus of each NLR and this creates a pore in the membrane which allows leakage of ions to occur and thus the cell dies.
Recent research suggests that they require CC-NLR proteins downstream of them, which are then activated to form the resistosomes and induce HR.
[22] Accidental activation of HR through the NLR proteins could cause vast destruction of the plant tissue, thus, the NLRs are kept in an inactive form through tight negative regulation at both transcriptional and post-translational levels.
[14] Mutations in certain components of plant defence machinery result in HR being activated without the presence of pathogen effector proteins.
[25] The mechanisms behind the influence of temperature on plant resistance to pathogens are not understood in detail, however, research suggests that the NLR protein levels might be important in this regulation.
[26] It is also proposed that at higher temperatures the NLR proteins are less likely to form oligomeric complexes, thus inhibiting their ability to induce HR.
[27] It has also been shown that HR is dependent on the light conditions, which could be linked to the activity of chloroplasts and mainly their ability to generate ROS.
For example, copper amine oxidase, catalyzes the oxidative deamination of polyamines, especially putrescine, and releases the ROS mediators hydrogen peroxide and ammonia.
These compounds may act by puncturing bacterial cell walls; or by delaying maturation, disrupting metabolism, or preventing reproduction of the pathogen in question.
Studies have suggested that the actual mode and sequence of the dismantling of plant cellular components depends on each individual plant-pathogen interaction, but all HR seem to require the involvement of cysteine proteases.
The induction of cell death and the clearance of pathogens also requires active protein synthesis, an intact actin cytoskeleton, and the presence of salicylic acid.
Pathogen-inducible promoters have been linked to auto-active NLR genes to induce HR response only when the pathogen is present but not at any other time.
It seems that in both plants and animals, the formation of the resistosome or the inflammasome, respectively, leads to cell death by forming pores in the membrane.
