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Plant disease resistance protects plants from pathogens in two ways: by pre-formed mechanisms and by infection-induced responses of the 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. Plants are almost always resistant to certain pathogens but susceptible to other pathogens; resistance is usually pathogen species-specific or pathogen strain-specific.


Plant disease resistance is crucial to the reliable production of food, and it provides significant reductions in agricultural use of land, water, fuel and other inputs. Plants in both natural and cultivated populations carry inherent disease resistance, but there are numerous examples of devastating plant disease impacts (see Irish Potato Famine, Chestnut blight), as well as recurrent severe plant diseases (see Rice blast, Soybean cyst nematode, Citrus canker). However, disease control is reasonably successful for most crops. Disease control is achieved by use of plants that have been bred for good resistance to many diseases, and by plant cultivation approaches such as crop rotation, use of pathogen-free seed, appropriate planting date and plant density, control of field moisture, and pesticide use. Across large regions and many crop species, it is estimated that diseases typically reduce plant yields by 10% every year in more developed nations or agricultural systems, but yield loss to diseases often exceeds 20% in less developed settings.

Common mechanisms[edit]

Pre-formed structures and compounds that contribute to resistance prior to immune response[edit]

secondary plant wall
  • 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 defences[1]

Inducible plant defenses that are generated after infection[edit]

  • 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 defence mediated by “Resistance genes.”[1]
  • Endophyte assistance: Plant's roots release chemicals that attract beneficial bacteria to fight off infections.[2]

Plant immune systems[edit]

Plant immune systems show some mechanistic similarities with the immune systems of insects and mammals, but also exhibit many plant-specific characteristics. Plants can sense the presence of pathogens and the effects of infection via different mechanisms than animals.[3] 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 many other responses that can directly activate cellular changes (such as cell wall reinforcement or the production of antimicrobial compounds), or activate changes in gene expression that then elevate plant defense responses.

Two major types of pathogen detection systems are observed in plant immune systems: PAMP-Triggered Immunity (PTI; also known as MAMP-triggered immunity or MTI), and Effector-Triggered Immunity (ETI).[4][5] The two systems detect different types of pathogen molecules, and tend to utilize different classes of plant receptor proteins to activate antimicrobial defenses. Although many specific examples of plant-pathogen detection mechanisms are now known that defy clear classification as PTI or ETI,[6] the larger trend across many well-studied plant-pathogen interactions supports continued use of PTI/ETI concepts.

Types of plant immunity[edit]

PAMP triggered immunity[edit]

The branch of the plant immune system pathogen detection system widely referred to as PAMP-Triggered Immunity (PTI) is often the first inducible response of a plant to a pathogen.[4][7] 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. Much less widely conserved molecules that nevertheless can be found in multiple pathogen genera are also classified as MAMPs by some researchers. 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 such as PTI.[5]

Effector triggered immunity[edit]

The Effector Triggered Immunity (ETI) branch of plant immune system pathogen detection systems is activated by the presence of pathogen effectors.[4][7] ETI is typically a very strong immune response that is reliant on R genes, and is activated by specific strains of pathogen species. As with PTI, many specific examples of apparent ETI defy portions of the common PTI/ETI definitions.[6] However, most plant immune systems carry a repertoire of 100-600 different R genes that mediate resistance against various virus, bacteria, fungus, oomycete and nematode pathogens, and against some insects. Plant ETI often causes a hypersensitive response - a programmed cell death response.

R genes and R proteins[edit]

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.[4] These virulence factors drove co-evolution of plant resistant genes to combat the pathogens’ Avr (avirulence) genes. Many but not all R genes encode NB-LRR proteins (nucleotide-binding/leucine-rich repeat domains, also known as NLR proteins, STAND proteins, among other names). 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, suggesting a receptor/ligand interaction for Avr and R genes.[7] Plant breeders frequently rely on R genes to obtain useful plant disease resistance, although the durability of this resistance can vary greatly depending on the specific pathogen, pathogen effector and R gene. 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.[8]

Effector biology[edit]

Effectors are central to the pathogenic or symbiotic potential of plant- and animal-associated microbes, and of microscopic plant-colonizing animals such as nematodes.[9][10][11] Effectors typically are proteins that are delivered outside of the microbe and into the host cell, although some effectors act outside of the host cell. Effectors manipulate plant cell physiology and development. As such, effectors offer examples of co-evolution (example: a fungal protein that functions outside of the fungus but inside of plant cells has evolved to take on plant-specific functions). Pathogen host range is determined, among other things, by the presence of an appropriate set of effectors that allows colonization of a particular host.[5] Pathogen-derived effectors are a powerful tool to identify host functions that are important in disease and disease resistance, as the apparent function of most effectors is to manipulate host physiology to allow disease to occur. Well-studied bacterial plant pathogens typically express a few dozen different effectors, often delivered into the host by a Type III secretion apparatus.[9] Fungal, oomycete, and nematode plant pathogens apparently express a few hundred different effectors.[10][11]

RNA silencing and systemic acquired resistance elicited by prior infections[edit]

Against viruses, plants often induce pathogen-specific gene silencing mechanisms mediated by RNA interference. This is a simple form of adaptive immunity.[12]

Plant immune systems also can 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.[13]

Defense against whole pathogen species[edit]

In a small number of cases, plant genes have been identified that are broadly effective against an entire pathogen species (against a microbial species 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 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.[citation needed]

Signaling mechanisms[edit]

Perception of pathogen presence[edit]

Plant defense signaling is activated by receptors that detect the presence of pathogens.[5] The activated receptors frequently elicit reactive oxygen and nitric oxide production, calcium, potassium and proton ion fluxes, altered levels of salicylic acid and other hormones, and activation of MAP kinases and other specific protein kinases.[7] These events in turn typically lead to the modification of proteins that control gene transcription, and the activation of defense-associated gene expression.

Pathogen perception via PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI) are described above. In addition to these common microbe-associated compounds (MAMPs, also called PAMPs), and pathogen effectors, plant defenses can also be activated by the sensing of damage-associated compounds (DAMPs, such as portions of the plant cell wall released during pathogenic infection). Many receptors for MAMPs, effectors and DAMPs have been discovered. Effectors are often detected by R gene-encoded NB-LRR proteins (nucleotide-binding/leucine-rich repeat proteins, also known as NLR proteins), while MAMPs and DAMPs are often detected by transmembrane receptor-kinases that carry LRR or LysM extracellular domains.[5]

Transcription factors and the hormone response[edit]

Numerous genes and/or proteins have been identified that mediate plant defense signal transduction.[14] Cytoskeleton and vesicle trafficking dynamics help to target plant defense responses asymmetrically within plant cells, toward the point of pathogen attack.

Mechanisms of transcription factors and hormones[edit]

Plant immune system activity is regulated in part by signaling hormones such as:[15]

There can be substantial cross-talk between these pathways[15]

Regulation by degradation[edit]

As with many signal transduction pathways, the plant's gene expression during immune responses can be regulated in part by degradation. This often occurs when hormone binding to hormone receptors stimulates ubiquitin-associated degradation of repressor proteins that block expression of certain genes. The net result is hormonal activation of expression of those genes. Some examples of these hormones are:[16]

  • Auxin: binds to receptors that then recruit and degrade repressors of transcriptional activators that stimulate auxin-specific gene expression.
  • Jasmonic acid: similar to auxin (see directly above), except with jasmonate receptors impacting jasmonate-response signaling mediators such as JAZ proteins.
  • Gibberellic acid: Gibberellin causes receptor conformational changes, and binding and degradation of Della proteins.
  • Ethylene: Inhibitory phosphorylation of the EIN2 ethylene response activator is blocked by ethylene binding. When this phosphorylation is reduced, EIN2 protein is cleaved and a portion of the protein moves to the nucleus to activate ethylene-response gene expression.

Mechanisms common to both plant and animal immune systems[edit]

The use of MAMP (PAMP) transmembrane receptors carrying leucine-rich repeat (LRR) pathogen recognition specificity domains, and of cytoplasmic NB-LRR or NLR receptors, is common to plant, insect, jawless vertebrate and mammal immune systems. The presence of Toll/Interleukin receptor (TIR) domains in plant immune receptors and also the expression of defensins, thionins, oxidative burst and other defense responses also reveal the presence of some common mechanisms shared between plant and animal immune systems.[4][17]

Ubiquitin and E3 signaling[edit]

Ubiquitination is a central role in cell signaling that regulates several processes including protein degradation and immunological response.[18] Much of the defense in plants relies on the destruction of defective or invaded materials within the cell, increasing the importance of functional proteasomes and protein targeting.[19] Although one of the main functions of ubiquitin is to target proteins for destruction, it is also useful in signaling pathways, hormone release, apoptosis, and translocation of materials throughout the cell. Ubiquitination is a key factor in several immune responses that are vital for the organism's survival. Without ubiquitin's proper functioning, the invasion of pathogens and other harmful molecules would increase dramatically due to weakened defenses in the plant's immunity.[18]

The E3 Ubiquitin ligase enzyme is the main component that provides specificity in the regulation of immune signaling pathways.[16] The E3 enzymes components are determined by which domains they contain and range from several types.[20] These include the Ring and U-box single subunit, HECT, and CRLs.[21][22] These plant signaling pathways are controlled by several feedback pathways, mainly negative feedback pathways; and they are regulated by De-ubiquitination enzymes, degradation of transcription factors, and the activation of transcription factors.[16]

E3 ubiquitin ligases have various roles in the ubiquitin pathway for immune signaling, which include plant defenses. The E3 role in ubiquitination and signaling is of major importance in the immune response, and the primary functioning of the enzymes include the following:[23]

This image depicts the pathways taken during responses in plant immunity. It highlights the role and effect ubiquitin has in regulating the pathway.
  • Regulators of hypersensitive cell death
  • Regulators of plant resistance
  • Regulators of PAMP (PAMP-Triggered Immunity)
  • Regulators of SAR (System Acquired Response)
  • Regulators of transcription factors
  • Regulators of hormone response

E2 signaling[edit]

Although E3 ubiquitin ligase has been demonstrated to be the most significant part of substrate specificity,[20] research has led scientists to believe that the other enzymes could play a key factor in plant signaling as well. A different family of genes containing the beta-grasp domain that resembles ubiquitin, known as ubiquitin-fold, supports this idea. One of the ubiquitin-fold proteins, Membrane-anchored Ubiquitin-fold (MUB), has been shown to aid in subcellular localization of the E2 conjugating enzyme.[24] This could be another important mechanism to examine in future studies for plant signaling and cellular processes.

Plant breeding for disease resistance[edit]

Plant breeders focus a significant part of their effort on selection and development of disease-resistant plant lines. Plant diseases can also be partially controlled by use of pesticides, and by cultivation practices such as crop rotation, tillage, planting density, purchase of disease-free seeds and cleaning of equipment, but plant varieties with inherent (genetically determined) disease resistance are generally the first choice for disease control. Breeding for disease resistance has been underway since plants were first domesticated, but it requires continual effort. This is because pathogen populations are often under natural selection for increased virulence, new pathogens can be introduced to an area, cultivation methods can favor increased disease incidence over time, changes in cultivation practice can favor new diseases, changes in climate can favor new diseases, and plant breeding for other traits can disrupt the disease resistance that was present in older plant varieties. A plant line with acceptable disease resistance against one pathogen may still lack resistance against other pathogens.

Plant breeding for disease resistance typically includes:

  • Identification of resistant breeding sources (plants that may be less desirable in other ways, but which carry a useful disease resistance trait). Ancient plant varieties and wild relatives are very important to preserve because they are the most common sources of enhanced plant disease resistance.
  • Crossing of a desirable but disease-susceptible plant variety to another variety that is a source of resistance, to generate plant populations that mix and segregate for the traits of the parents.
  • Growth of the breeding populations in a disease-conducive setting. This may require artificial inoculation of pathogen onto the plant population. Careful attention must be paid to the types of pathogen isolates that are present, as there can be significant variation the effectiveness of resistance against different isolates of the same pathogen species.
  • Selection of disease-resistant individuals. Breeders are trying to sustain or improve numerous other plant traits related to plant yield and quality, including other disease resistance traits, while they are breeding for improved resistance to any particular pathogen.

Each of the above steps can be difficult to successfully accomplish, and many highly refined methods in plant breeding and plant pathology are used to increase the effectiveness and reduce the cost of resistance breeding.

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.

Crops such as potato, apple, banana and sugarcane are often propagated by vegetative reproduction to preserve highly desirable plant varieties, because for these species, outcrossing seriously disrupts the preferred plant varieties. See also asexual propagation. Vegetatively propagated crops may be among the best targets for resistance improvement by the biotechnology method of plant transformation to add individual genes that improve disease resistance without causing large genetic disruption of the preferred plant varieties.

Host range[edit]

See also: Plant pathology

There are thousands of species of plant pathogenic microorganisms, 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 pathogen's 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[edit]

Plants in native populations are often characterized by substantial genotype diversity and dispersed populations (growth in a mixture with many other plant species). They also have undergone millions of years of plant-pathogen coevolution. Hence as long as novel pathogens are not introduced from other parts of the globe, natural plant populations generally exhibit only a 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. Climate change can alter the viable geographic range of pathogen species and cause some diseases to become a problem in areas where the disease was previously less important. 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.[25]

See also[edit]



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  2. ^ Bryant, Tracy (2008). When under attack, plants can signal microbial friends for help. University of Delaware.
  3. ^ Boyd, Jade (2012). A bit touchy: Plants' insect defenses activated by touch. Rice University.
  4. ^ a b c d e Jones, J.D.; Dangl, J.L. (2006). "The plant immune system". Nature. 444: 323–329.  Cite uses deprecated parameter |coauthors= (help)
  5. ^ a b c d e Dodds, P. & Rathjen, J. 2010. Plant immunity: towards an integrated view of plant–pathogen interactions. Nature Reviews Genetics 11:539.
  6. ^ a b Thomma, B., Nurnberger, T. and Joosten, M. 2011. Of PAMPs and Effectors: The Blurred PTI-ETI Dichotomy. The Plant Cell 23:4–15.
  7. ^ a b c d Numberger, T.; Brunner, F., Kemmerling, B., and Piater, L. (2004). "Innate immunity in plants and animals: striking similarities and obvious differences". Immunological Reviews. 198: 249–266.  Cite uses deprecated parameter |coauthors= (help)
  8. ^ Friedman AR and Baker BJ. 2007. The evolution of resistance genes in multi-protein plant resistance systems. Curr Opin Genet Dev. 17:493-499.
  9. ^ a b Lindeberg M, Cunnac S, Collmer A. 2012. Pseudomonas syringae type III effector repertoires: last words in endless arguments. Trends Microbiol. 4:199-208.
  10. ^ a b Rafiqi M, Ellis JG, Ludowici VA, Hardham AR, Dodds PN. 2012. Challenges and progress towards understanding the role of effectors in plant-fungal interactions. Curr Opin Plant Biol. 15:477-82.
  11. ^ a b Hewezi T. and Baum, T.J. 2013. Manipulation of plant cells by cyst and root-knot nematode effectors. Mol. Plant Microbe Interact. 26:9-16.
  12. ^ Ding, S.W. and Voinnet, O. 2007. Antiviral immunity directed by small RNAs. Cell 130:413-26.
  13. ^ Spoel, S.H. and Dong, X. 2012. How do plants achieve immunity? Defence without specialized immune cells. Nature Reviews Immunology 12:89-100.
  14. ^ Hammond-Kosack KE and Parker JE. 2003. Deciphering plant-pathogen communication: fresh perspectives for molecular resistance breeding. Curr Opin Biotechnol. 14:177-193
  15. ^ a b Moore, J. W.; Loake, G. J.; Spoel, S. H. (12 August 2011). "Transcription Dynamics in Plant Immunity". The Plant Cell. 23 (8): 2809–2820. doi:10.1105/tpc.111.087346.  Cite uses deprecated parameter |coauthors= (help)
  16. ^ a b c Sadanandom, Ari; Bailey, Mark; Ewan, Richard; Lee, Jack; Nelis, Stuart (1 October 2012). "The ubiquitin-proteasome system: central modifier of plant signalling". New Phytologist. 196 (1): 13–28. doi:10.1111/j.1469-8137.2012.04266.x.  Cite uses deprecated parameter |coauthors= (help)
  17. ^ Ting JP et al. 2008. NLRs at the intersection of cell death and immunity. Nat Rev Immunol. 8:372-379
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  21. ^ Moon, J. (1 December 2004). "The Ubiquitin-Proteasome Pathway and Plant Development". THE PLANT CELL ONLINE. 16 (12): 3181–3195. doi:10.1105/tpc.104.161220. 
  22. ^ Trujillo, Marco; Shirasu, Ken (1 August 2010). "Ubiquitination in plant immunity". Current Opinion in Plant Biology. 13 (4): 402–408. doi:10.1016/j.pbi.2010.04.002.  Cite uses deprecated parameter |coauthors= (help)
  23. ^ Shirsekar, Gautam; Dai, Liangying; Hu, Yajun; Wang, Xuejun; Zeng, Lirong; Wang, Guo-Liang (NaN undefined NaN). "Role of Ubiquitination in Plant Innate Immunity and Pathogen Virulence". Journal of Plant Biology. 53 (1): 10–18. doi:10.1007/s12374-009-9087-x.  Cite uses deprecated parameter |coauthors= (help); Check date values in: |date= (help)
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  25. ^ McDonald BA and Linde C. 2002. Pathogen population genetics, evolutionary potential, and durable resistance. Annu Rev Phytopathol. 2002;40:349-79.

Further reading[edit]

  • Lucas, J.A., "Plant Defence." Chapter 9 in Plant Pathology and Plant Pathogens, 3rd ed. 1998 Blackwell Science. ISBN 0-632-03046-1
  • Hammond-Kosack, K. and Jones, J.D.G. "Responses to plant pathogens." In: Buchanan, Gruissem and Jones, eds. Biochemistry and Molecular Biology of Plants. 2000 Amer.Soc.Plant Biol., Rockville, MD. ISBN 0-943088-39-9
  • Dodds, P. & Rathjen, J. 2010. Plant immunity: towards an integrated view of plant–pathogen interactions. Nature Reviews Genetics 11:539.
  • Schumann, G. Plant Diseases: Their Biology and Social Impact. 1991 APS Press, St. Paul, MN ISBN 0-89054-16-7

External links[edit]