Hypersensitive response

For hypersensitivity response in humans, see Hypersensitivity.

The hypersensitive response (HR) is a mechanism, used by plants, to prevent the spread of infection by microbial pathogens. The HR is characterized by the rapid death of cells in the local region surrounding an infection. The HR serves to restrict the growth and spread of pathogens to other parts of the plant. The HR is analogous to the innate immune system found in animals, and commonly precedes a slower systemic (whole plant) response, which ultimately leads to systemic acquired resistance (SAR).[1]

Mechanism

The HR is triggered by the plant when it recognizes a pathogen. The identification of a pathogen typically occurs when avirulence geneproducts, secreted by a pathogen, bind to, or indirectly interact with the product of a plant resistance (R) gene (gene for gene model). R genes are highly polymorphic, and many plants produce several different types of R gene products, enabling them to recognize virulence products produced by many different pathogens.[2]

In phase one of the HR, the activation of R genes triggers an ion flux, involving an efflux of hydroxide and potassium outside the cells, and an influx of calcium and hydrogen ions into the cell.[3]

In phase two, the cells involved in the HR generate an oxidative burst by producing reactive oxygen species (ROS), superoxide anions, hydrogen peroxide, hydroxyl radicals and nitrous oxide. These compounds affect cellular membrane function, in part by inducing lipid peroxidation and by causing lipid damage.[3]

The alteration of ion components in the cell, and the breakdown of cellular components in the presence of ROS, results in the death of affected cells and the formation of local lesions. 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.[3] These compounds serve to reinforce the walls of cells surrounding the infection, creating a barrier and inhibiting the spread of the infection.[4]

Mediators

Several enzymes have been shown to be involved in generation of ROS. For example, copper amine oxidase, catalyzes the oxidative deamination of polyamines, especially putrescine, and releases the ROS mediators hydrogen peroxide and ammonia.[5] Other enzymes thought to play a role in ROS production include xanthine oxidase, NADPH oxidase, oxalate oxidase, peroxidases, and flavin containing amine oxidases. [3]

In some cases, the cells surrounding the lesion synthesize antimicrobial compounds, including phenolics, phytoalexins, and pathogenesis related (PR) proteins, including β-glucanases and chitinases. 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.[2]

Pathogen evasion

Pathogens have evolved several strategies designed to suppress plant defense responses. Host processes usually targeted by bacteria include; alterations to programmed cell death pathways, inhibiting cell wall-based defenses, and altering plant hormone signaling and expression of defense genes.[6]

See also

References

  1. ↑ Freeman, Scott (2003). Chapter 37: Plant Defense Systems. Prentice Hall.
  2. 1 2 Heath, MC. (2000). "Hypersensitive response-related death.". Plant Molecular Biology. 44 (3): 321–34. doi:10.1023/A:1026592509060. PMID 11199391.
  3. 1 2 3 4 Matthews, Ben. "The Hypersensitive Response". Agricultural Research Service: Plant Science Institute. The United States Department of Agriculture. Retrieved 2007-01-12.
  4. ↑ Pontier, D,; Balague C; Roby D. (1998). "The hypersensitive response. A programmed cell death associated with plant resistance". C R Acad Sci III. 321 (9): 721–34. doi:10.1016/s0764-4469(98)80013-9. PMID 9809204.
  5. ↑ Koyanagi, T; Matsumura K; Kuroda S; Tanizawa K. (2000). "Molecular cloning and heterologous expression of pea seedling copper amine oxidase.". Biosci Biotechnol Biochem. 64 (4): 717–22. doi:10.1271/bbb.64.717. PMID 10830482.
  6. ↑ Abramovitch, RB; GB Martin (2004). "Strategies used by bacterial pathogens to suppress plant defenses.". Current Opinion in Plant Biology. 7 (4): 356–64. doi:10.1016/j.pbi.2004.05.002. PMID 15231256.
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