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Plant Disease Resistance (the resistance of plants to infectious diseases) derives both from pre-formed defenses and from infection-induced responses mediated by the plant immune system. Relative to a disease-susceptible plant, disease resistance is often defined as reduction of pathogen growth on or in the plant, while the term disease tolerance describes plants that exhibit less disease damage despite similar levels of pathogen growth. Disease outcome is determined by the three-way interaction of the pathogen, the plant, and the environmental conditions (an interaction known as the disease triangle). Defense-activating compounds can move cell-to-cell and systemically through the plant vascular system, but plants do not have circulating immune cells so most cell types in plants retain the capacity to express a broad suite of antimicrobial defenses. Although obvious qualitative differences in disease resistance can be observed when some plants are compared (allowing classification as “resistant” or “susceptible” after infection by the same pathogen strain at similar pathogen inoculum levels in similar environments), a gradation of quantitative differences in disease resistance is more typically observed between plant lines or genotypes.

Note that plant defense against herbivory (plant resistance to insect pests) exhibits some mechanistic similarities to, but also differences from, plant disease resistance (plant resistance to microscopic organisms).

==Common Mechanisms of Plant Disease Resistance ==

Pre-formed structures and compounds that contribute to resistance:

 * Plant cuticle/surface
 * Plant cell walls
 * Antimicrobial chemicals (for example: glucosides, saponins)
 * Antimicrobial proteins
 * Enzyme inhibitors
 * Detoxifying enzymes that break down pathogen-derived toxins
 * Receptors that perceive pathogen presence and activate inducible plant defenses

Inducible plant defenses that are generated after infection:

 * Cell wall reinforcement (callose, lignin, suberin, cell wall proteins)
 * Antimicrobial chemicals (including reactive oxygen species such as hydrogen peroxide, or peroxynitrite, or more complex phytoalexins such as genistein or camalexin)
 * Antimicrobial proteins such as defensins, thionins, or PR-1
 * Antimicrobial enzymes such as chitinases, beta-glucanases, or peroxidases
 * Hypersensitive response - a rapid host cell death response associated with defense mediated by “Resistance genes.”

Plant Immune Systems and Plant Defense Signal Transduction
Plant immune systems show some mechanistic similarities and apparent common origin with the immune systems of insects and mammals, but also exhibit many plant-specific characteristics. As in most cellular responses to the environment, defenses are activated when receptor proteins directly or indirectly detect pathogen presence and trigger ion channel gating, oxidative burst, cellular redox changes, protein kinase cascades, and/or other responses that either directly activate cellular changes (such as cell wall reinforcement), or activate changes in gene expression that then elevate plant defense responses.

Plants, like animals, have a basal immune system that includes a small number of pattern recognition receptors that are specific for broadly conserved microbe-associated molecular patterns (MAMPs, also called pathogen-associated molecular patterns or PAMPs). Examples of these microbial compounds that elicit plant basal defense include bacterial flagellin or lipopolysaccharides, or fungal chitin. The defenses induced by MAMP perception are sufficient to repel most potentially pathogenic microorganisms. However, pathogens express effector proteins that are adapted to allow them to infect certain plant species; these effectors often enhance pathogen virulence by suppressing basal host defenses.

Importantly, plants have evolved R genes (resistance genes) whose products allow recognition of specific pathogen effectors, either through direct binding of the effector or by recognition of the alteration that the effector has caused to a host protein. R gene products control a broad set of disease resistance responses whose induction is often sufficiently rapid and strong to stop adapted pathogens from further growth or spread. Plant genomes each contain a few hundred apparent R genes, and the R genes studied to date usually confer specificity for particular strains of a pathogen species. As first noted by Harold Flor in the mid-20th century in his formulation of the gene-for-gene relationship, the plant R gene and the pathogen “avirulence gene” (effector gene) must have matched specificity for that R gene to confer resistance. The presence of an R gene can place significant selective pressure on the pathogen to alter or delete the corresponding avirulence/effector gene. Some R genes show evidence of high stability over millions of years while other R genes, especially those that occur in small clusters of similar genes, can evolve new pathogen specificities over much shorter time periods.

The use of receptors carrying leucine-rich repeat (LRR) pathogen recognition specificity domains is common to plant, insect, jawless vertebrate and mammal immune systems, as is the presence of Toll/Interleukin receptor (TIR) domains in many of these receptors, and the expression of defensins, thionins, oxidative burst and other defense responses.

Some of the key endogenous chemical mediators of plant defense signal transduction include salicylic acid, jasmonic acid or jasmonate, ethylene, reactive oxygen species, and nitric oxide. Numerous genes and/or proteins have been identified that mediate plant defense signal transduction. Cytoskeleton and vesicle trafficking dynamics help to target plant defense responses asymmetrically within plant cells, toward the point of pathogen attack.

Plant immune systems can also respond to an initial infection in one part of the plant by physiologically elevating the capacity for a successful defense response in other parts of the plant. These responses include systemic acquired resistance, largely mediated by salicylic acid-dependent pathways, and induced systemic resistance, largely mediated by jasmonic acid-dependent pathways. Against viruses, plants often induce pathogen-specific gene silencing mechanisms mediated by RNA interference. These are primitive forms of adaptive immunity.

In a small number of cases, plant genes have been identified that are broadly effective against an entire pathogen species (against a that is pathogenic on other genotypes of that host species. Examples include barley MLO against powdery mildew, wheat Lr34 against leaf rust, and wheat Yr36 against stripe rust.  An array of mechanisms for this type of resistance may exist depending on the particular gene and plant-pathogen combination.  Other reasons for effective plant immunity can include a relatively complete lack of coadaptation (the pathogen and/or plant lack multiple mechanisms needed for colonization and growth within that host species), or a particularly effective suite of pre-formed defenses (see above).

Plant Breeding for Disease Resistance
Plant breeders focus a significant part of their effort on selection and development of disease-resistant plant lines. Plant diseases can also be controlled by use of pesticides, and by cultivation practices such as crop rotation, purchase of disease-free seeds and cleaning of equipment, but plant varieties with inherent (genetically determined) disease resistance are often very popular. Breeding for disease resistance requires continual effort because pathogen populations are often under natural selection for increased virulence, new pathogens can be introduced to an area, and plant breeding for other traits can disrupt the disease resistance that was present in older plant varieties. Resistance is termed durable if it continues to be effective over multiple years of widespread use, but some resistance “breaks down” as pathogen populations evolve to overcome or escape the resistance. Resistance that is specific to certain races or strains of a pathogen species is often controlled by single R genes and can be less durable; broad-spectrum resistance against an entire pathogen species is often quantitative and only incompletely effective, but more durable, and is often controlled by many genes that segregate in breeding populations. However, there are numerous exceptions to the above generalized trends, which were given the names vertical resistance and horizontal resistance, respectively, by J.E. Vanderplank.

Host Range
There are thousands of species of plant pathogenic microorganisms (see Plant Pathology), but only a small minority of these pathogens have the capacity to infect a broad range of plant species. Most pathogens instead exhibit a high degree of host-specificity. Non-host plant species are often said to express non-host resistance. The term host resistance is used when a pathogen species can be pathogenic on the host species but certain strains of that plant species resist certain strains of the pathogen species. There can be overlap in the causes of host resistance and non-host resistance. Pathogen host range can change quite suddenly if, for example, the capacity to synthesize a host-specific toxin or effector is gained by gene shuffling/mutation, or by horizontal gene transfer from a related or relatively unrelated organism.

Epidemics and Population Biology
Plants in native populations are often characterized by substantial genotype diversity and dispersed populations (growth in a mixture with many other plant species). This, together with millions of years of plant-pathogen coevolution, and/or rare introduction of novel pathogens from other parts of the globe, can lead to a relatively low incidence of severe disease epidemics. In agricultural systems, humans often cultivate single plant species at high density, with numerous fields of that species in a region, and with significantly reduced genetic diversity both within fields and between fields. In addition, rapid travel of people and cargo across large distances increases the risk of introducing pathogens against which the plant has not been selected for resistance. These factors make modern agriculture particularly prone to disease epidemics. Common solutions to this problem include constant breeding for disease resistance, use of pesticides to suppress recurrent potential epidemics, use of border inspections and plant import restrictions, maintenance of significant genetic diversity within the crop gene pool (see Crop diversity), and constant surveillance for disease problems to facilitate early initiation of appropriate responses. Some pathogen species are known to have a much greater capacity to overcome plant disease resistance than others, often because of their ability to evolve rapidly and to disperse broadly.