Plant disease resistance

Plant disease resistance protects plants from pathogens

in two ways: by preformed mechanisms and by infectioninduced responses of the immune system. Relative to
a susceptible plant, disease resistance is the reduction
of pathogen growth on or in the plant, while the term
disease tolerance describes plants that exhibit little disease damage despite substantial pathogen levels. 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).

in more developed nations or agricultural systems, but

yield loss to diseases often exceeds 20% in less developed
settings, an estimated 15% of global crop production.[1]
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,
pathogen-free seed, appropriate planting date and plant
density, control of eld moisture and pesticide use.

Defense-activating compounds can move cell-to-cell and

systemically through the plant vascular system. However,
plants do not have circulating immune cells, so most cell 2
types exhibit a broad suite of antimicrobial defenses. Although obvious qualitative dierences in disease resis- 2.1
tance can be observed when multiple specimens are compared (allowing classication as resistant or susceptible after infection by the same pathogen strain at similar
inoculum levels in similar environments), a gradation of
quantitative dierences in disease resistance is more typically observed between plant strains or genotypes. Plants
consistently resist certain pathogens but succumb to others; resistance is usually pathogen species- or pathogen
strain-specic.

Common mechanisms
Pre-formed structures and compounds

Background

Plant disease resistance is crucial to the reliable production of food, and it provides signicant reductions in agricultural use of land, water, fuel and other inputs. Plants secondary plant wall
in both natural and cultivated populations carry inherent
disease resistance, but this has not always protected them.
Plant cuticle/surface
The late blight Irish potato famine of the 1840s was
caused by the oomycete Phytophthora infestans. The
Plant cell walls
worlds rst mass-cultivated banana cultivar Gros Michel
was lost in the 1920s to Panama disease caused by the
Antimicrobial chemicals (for example: glucosides,
fungus Fusarium oxysporum. The current wheat stem,
saponins)
leaf, and yellow stripe rust epidemics spreading from East
Africa into the Indian subcontinent are caused by rust
Antimicrobial proteins
fungi Puccinia graminis and P. striiformis. Other epidemics include Chestnut blight), as well as recurrent se Enzyme inhibitors
vere plant diseases such as Rice blast, Soybean cyst nematode, Citrus canker.[1]
Detoxifying enzymes that break down pathogenderived toxins

Plant pathogens can spread rapidly over great distances,

vectored by water, wind, insects, and humans. Across
large regions and many crop species, it is estimated that
diseases typically reduce plant yields by 10% every year

Receptors that perceive pathogen presence and activate inducible plant defences[2]
1

2.2

IMMUNE SYSTEM

Inducible post-infection plant defenses 3.1 PAMP-triggered immunity

Cell wall reinforcement (callose, lignin, suberin, cell PAMP-Triggered Immunity (PTI) is often a plants rst
wall proteins)
inducible response.[4][7] Immune-eliciting PAMPs in Antimicrobial chemicals, including reactive oxygen clude bacterial agellin or lipopolysaccharides, or fungal
species such as hydrogen peroxide or peroxynitrite, chitin. Much less widely conserved molecules that inor more complex phytoalexins such as genistein or habit multiple pathogen genera are classied as MAMPs
by some researchers. The defenses induced by MAMP
camalexin)
perception are sucient to repel most pathogens. How Antimicrobial proteins such as defensins, thionins, ever, pathogen eector proteins are adapted to suppress
or PR-1
basal defenses such as PTI.[5]
Antimicrobial enzymes such as chitinases, betaglucanases, or peroxidases

3.2 Eector triggered immunity

Hypersensitive response - a rapid host cell death response associated with defence mediated by Resis- Eector Triggered Immunity (ETI) is activated by the
tance genes.[2]
presence of pathogen eectors.[4][7] The ETI immune response is reliant on R genes, and is activated by specic
Endophyte assistance: Plants roots release chempathogen strains. As with PTI, many specic examples
icals that attract benecial bacteria to ght o
of apparent ETI violate common PTI/ETI denitions.[8]
[3]
infections.
Most plant immune systems carry a repertoire of 100-600
dierent R genes that mediate resistance to various virus,
bacteria, fungus, oomycete and nematode pathogens and
3 Immune system
insects. Plant ETI often cause an apoptotic hypersensitive
response.
The plant immune system consists of two interconnected
tiers of receptors, one outside and one inside the cell.
Both systems sense the intruder, respond to the intrusion 3.2.1 R genes and R proteins
and optionally signal to the rest of the plant and sometimes to neighboring plants that the intruder is present. Plants have evolved R genes (resistance genes) whose
The two systems detect dierent types of pathogen products allow recognition of specic pathogen eectors,
either through direct binding or by recognition of the efmolecules and classes of plant receptor proteins.[1]
fectors alteration of a host protein.[4] These virulence
The rst tier is primarily governed by pattern recognition factors drove co-evolution of plant resistant genes to comreceptors that are activated by recognition of evolutionar- bat the pathogens Avr (avirulent) genes. Many R genes
ily conserved pathogen or microbialassociated molecu- encode NB-LRR proteins (nucleotide-binding/leucinelar patterns (PAMPs or MAMPs, here P/MAMP). Ac- rich repeat domains, also known as NLR proteins or
tivation of PRRs leads to intracellular signaling, tran- STAND proteins, among other names).
scriptional reprogramming, and biosynthesis of a complex output response that limits colonization. The system R gene products control a broad set of disease resistance
responses whose induction is often sucient to stop furis known as PAMP-Triggered Immunity (PTI).[4][5]
ther pathogen growth/spread. Each plant genome conThe second tier (again, primarily), eector-triggered imtains a few hundred apparent R genes. Studied R genes
munity (ETI), consists of another set of receptors, the usually confer specicity for particular pathogen strains.
nucleotide-binding LRRs (NLRs). They operate within
As rst noted by Harold Flor in his mid-20th century
the cell, encoded by R genes. The presence of specic formulation of the gene-for-gene relationship, the plant
pathogen eectors activates specic NLR proteins that R gene and the pathogen Avr gene must have matched
limit pathogen proliferation.[1]
specicity for that R gene to confer resistance, suggesting
Receptor responses include ion channel gating, oxidative a receptor/ligand interaction for Avr and R genes.[7] Alburst, cellular redox changes, or protein kinase cascades ternatively, an eector can modify its host cellular target
that directly activate cellular changes (such as cell wall (or a molecular decoy of that target) activating an NLR
reinforcement or antimicrobial production), or activate associated with the target or decoy.
changes in gene expression that then elevate other defen- Plant breeders frequently rely on R genes to obtain usesive responses.[1]
ful resistance, although the durability of this resistance
Plant immune systems show some mechanistic similarities with the immune systems of insects and mammals, but also exhibit many plant-specic characteristics.
Plants can sense the presence of pathogens and the eects
of infection via dierent mechanisms than animals.[6]

can vary by pathogen, pathogen eector and R gene. The

presence of an R gene can place signicant selective pressure on the pathogen to alter or delete the corresponding
avirulence/eector gene. Some R genes show evidence of
stability over millions of years while other R genes, espe-

3
cially those that occur in small clusters of similar genes, type of resistance may exist depending on the particcan evolve new pathogen specicities over much shorter ular gene and plant-pathogen combination. Other reaintervals.[9]
sons for eective plant immunity can include a lack of
coadaptation (the pathogen and/or plant lack multiple
mechanisms needed for colonization and growth within
3.2.2 Eector biology
that host species), or a particularly eective suite of preformed defenses.
Eectors are central to microbes pathogenic or symbiotic potential and of microscopic plant-colonizing animals such as nematodes.[10][11][12] Eectors typically are
proteins that are delivered mostly outside the microbe 4 Signaling mechanisms
and into the host cell. Eectors manipulate cell physiology and development. As such, eectors oer exam- 4.1 Perception of pathogen presence
ples of co-evolution (example: a fungal protein that functions outside of the fungus but inside of plant cells has Plant defense signaling is activated by pathogen-detecting
evolved to take on plant-specic functions). Pathogen receptors.[5] The activated receptors frequently elicit
host range is determined, among other things, by the pres- reactive oxygen and nitric oxide production, calcium,
ence of appropriate eectors that allow colonization of a potassium and proton ion uxes, altered levels of salicylic
particular host.[5] Pathogen-derived eectors are a pow- acid and other hormones and activation of MAP kinases
erful tool to identify host functions that are important in and other specic protein kinases.[7] These events in turn
disease. Apparently most eectors function to manip- typically lead to the modication of proteins that conulate host physiology to allow disease to occur. Well- trol gene transcription, and the activation of defensestudied bacterial plant pathogens typically express a few associated gene expression.
dozen eectors, often delivered into the host by a Type
III secretion apparatus.[10] Fungal, oomycete and nema- In addition to PTI and ETI, plant defenses can be actitode plant pathogens apparently express a few hundred vated by the sensing of damage-associated compounds
(DAMP), such as portions of the plant cell wall reeectors.[11][12]
leased during pathogenic infection. Many receptors for
So-called core eectors are dened operationally by MAMPs, eectors and DAMPs have been discovered.
their wide distribution across the population of a par- Eectors are often detected by NLRs, while MAMPs and
ticular pathogen and their substantial contribution to DAMPs are often detected by transmembrane receptorpathogen virulence. Genomics can be used to identify kinases that carry LRR or LysM extracellular domains.[5]
core eectors, which can then functionally dene new R
alleles, which can serve as breeding targets.[1]

3.3

4.2 Transcription factors and the hormone

response
RNA silencing and systemic acquired
resistance elicited by prior infections

Numerous genes and/or proteins have been identied that mediate plant defense signal transduction.[15]
Against viruses, plants often induce pathogen-specic
Cytoskeleton and vesicle tracking dynamics help to origene silencing mechanisms mediated by RNA interferent plant defense responses toward the point of pathogen
[13]
ence. This is a simple form of adaptive immunity.
attack.
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 4.2.1 Mechanisms of transcription factors and horparts. Such responses include systemic acquired resismones
tance, largely mediated by salicylic acid-dependent pathways, and induced systemic resistance, largely mediated Plant immune system activity is regulated in part by sigby jasmonic acid-dependent pathways.[14]
naling hormones such as:[16]

3.4

Species-level resistance

Salicylic acid

Jasmonic acid
In a small number of cases, plant genes are eective
against an entire pathogen species, even though that
Ethylene
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 There can be substantial cross-talk among these
against stripe rust. An array of mechanisms for this pathways.[16]

5 PLANT BREEDING FOR DISEASE RESISTANCE

4.3

Regulation by degradation

As with many signal transduction pathways, plant gene

expression during immune responses can be regulated 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 hormone-activated gene expression. Examples:[17]
Auxin: binds to receptors that then recruit and degrade repressors of transcriptional activators that
stimulate auxin-specic gene expression.
Jasmonic acid: similar to auxin, 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.

This image depicts the pathways taken during responses in plant

immunity. It highlights the role and eect ubiquitin has in regulating the pathway.

4.4 Mechanisms common to both plant

Ethylene: Inhibitory phosphorylation of the EIN2

and animal immune systems
ethylene response activator is blocked by ethylene
binding. When this phosphorylation is reduced,
EIN2 protein is cleaved and a portion of the protein The use of PAMP transmembrane receptors carrying
moves to the nucleus to activate ethylene-response leucine-rich repeat (LRR) pathogen recognition specicity domains, and of cytoplasmic NB-LRR or NLR
gene expression.
receptors, is common to plant, insect, jawless vertebrate and mammal immune systems. The presence of
Toll/Interleukin receptor (TIR) domains in plant immune
4.3.1 Ubiquitin and E3 signaling
receptors and also the expression of defensins, thionins,
oxidative burst and other defense responses also reveal the
Ubiquitination plays a central role in cell signaling that presence of mechanisms shared between plant and animal
regulates processes including protein degradation and immune systems.[4][23]
immunological response.[18] 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 5 Plant breeding for disease resisthe cell. Ubiquitination is a component of several imtance
mune responses. Without ubiquitins proper functioning,
the invasion of pathogens and other harmful molecules
would increase dramatically due to weakened immune Plant breeders emphasize selection and development of
defenses.[18]
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 denE3 signaling
The E3 Ubiquitin ligase enzyme is sity, disease-free seeds and cleaning of equipment, but
a main component that provides specicity in pro- plant varieties with inherent (genetically determined) distein degradation pathways, including immune signal- ease resistance are generally preferred. Breeding for dising pathways.[17] The E3 enzyme components can be ease resistance began when plants were rst domestigrouped by which domains they contain and include sev- cated. Breeding eorts continue because pathogen poperal types.[19] These include the Ring and U-box single ulations are under selection pressure for increased virusubunit, HECT, and CRLs.[20][21] Plant signaling path- lence, new pathogens appear, evolving cultivation pracways including immune responses are controlled by sev- tices and changing climate can reduce resistance and/or
eral feedback pathways, which often include negative strengthen pathogens, and plant breeding for other traits
feedback; and they can be regulated by De-ubiquitination can disrupt prior resistance. A plant line with acceptenzymes, degradation of transcription factors and the able resistance against one pathogen may lack resistance
degradation of negative regulators of transcription.[17][22] against others.

5.1

GM or transgenic engineered disease resistance

Breeding for resistance typically includes:

Identication of plants that may be less desirable in
other ways, but which carry a useful disease resistance trait, including wild strains that often express
enhanced resistance.

5
viral coat protein gene sequences conferred virus resistance via small RNAs. This proved to be a widely applicable mechanism for inhibiting viral replication. Combining coat protein genes from three dierent viruses,
scientists developed squash hybrids with eld-validated,
multiviral resistance. Similar levels of resistance to this
variety of viruses had not been achieved by conventional
breeding.

Crossing of a desirable but disease-susceptible variety to another variety that is a source of resistance. A similar strategy was deployed to combat papaya
ringspot virus, which by 1994 threatened to destroy
Growth of breeding candidates in a disease- Hawaiis papaya industry. Field trials demonstrated exconducive setting, possibly including pathogen in- cellent ecacy and high fruit quality. By 1998 the rst
oculation. Attention must be paid to the specic transgenic virus-resistant papaya was approved for sale.
pathogen isolates, to address variability within a sin- Disease resistance has been durable for over 15 years.
gle pathogen species.
Transgenic papaya accounts for ~85% of Hawaiian production. The fruit is approved for sale in the U.S., Canada
Selection of disease-resistant individuals that retain and Japan.
other desirable traits such as yield, quality and inPotato lines expressing viral replicase sequences that concluding other disease resistance traits.
fer resistance to potato leafroll virus were sold under the
trade names NewLeaf Y and NewLeaf Plus, and were
Resistance is termed durable if it continues to be eec- widely accepted in commercial production in 1999-2001,
tive over multiple years of widespread use as pathogen until McDonalds Corp. decided not to purchase GM
populations evolve. "Vertical resistance" is specic to potatoes and Monsanto decided to close their Naturecertain races or strains of a pathogen species, is often Mark potato business.[25] NewLeaf Y and NewLeaf Plus
controlled by single R genes and can be less durable. potatoes carried two GM traits, as they also expressed BtHoizontal or broad-spectrum resistance against an entire mediated resistance to Colorado potato beetle.
pathogen species is often only incompletely eective, but
more durable, and is often controlled by many genes that No other crop with engineered disease resistance against
microbial pathogens had reached the market by 2013, alsegregate in breeding populations.
though more than a dozen were in some state of developCrops such as potato, apple, banana and sugarcane are ment and testing.
often propagated by vegetative reproduction to preserve
highly desirable plant varieties, because for these species,
outcrossing seriously disrupts the preferred traits. See 5.1.1 PRR transfer
also asexual propagation. Vegetatively propagated crops
may be among the best targets for resistance improvement Research aimed at engineered resistance follows multiby the biotechnology method of plant transformation to ple strategies. One is to transfer useful PRRs into species
manage genes that aect disease resistance.
that lack them. Identication of functional PRRs and
Scientic breeding for disease resistance originated with their transfer to a recipient species that lacks an ortholSir Rowland Bien, who identied a single recessive gene ogous receptor could provide a general pathway to adfor resistance to wheat yellow rust. Nearly every crop was ditional broadened PRR repertoires. For example, the
then bred to include disease resistance (R) genes, many by Arabidopsis PRR EF-Tu receptor (EFR) recognizes the
bacterial translation elongation factor EF-Tu. Research
introgression from compatible wild relatives.[1]
performed at Sainsbury Laboratory demonstrated that deployment of EFR into either Nicotiana benthamianaor
5.1 GM or transgenic engineered disease Solanum lycopersicum (tomato), which cannot recognize
EF-Tu, conferred resistance to a wide range of bacteresistance
rial pathogens. EFR expression in tomato was especially eective against the widespread and devastating
The term GM (genetically modied) is often used soil bacterium Ralstonia solanacearum.[26] Conversely,
as a synonym of transgenic to refer to plants modi- the tomato PRR Verticillium 1 (Ve1) gene can be transed using recombinant DNA technologies. Plants with ferred from tomato to Arabidopsis, where it confers resistransgenic/GM disease resistance against insect pests tance to race 1 Verticillium isolates.[1]
have been extremely successful as commercial products, especially in maize and cotton, and are planted
annually on over 20 million hectares in over 20 coun- 5.1.2 Stacking
tries worldwide[24] (see also genetically modied crops).
Transgenic plant disease resistance against microbial The second strategy attempts to deploy multiple NLR
pathogens was rst demonstrated in 1986. Expression of genes simultaneously, a breeding strategy known as

6
stacking. Cultivars generated by either DNA-assisted
molecular breeding or gene transfer will likely display
more durable resistance, because pathogens would have
to mutate multiple eector genes. DNA sequencing allows researchers to functionally mine NLR genes from
multiple species/strains.[1]
The avrBs2 eector gene from Xanthomona perforans is
the causal agent of bacterial spot disease of pepper and
tomato. The rst eector-rationalized search for a potentially durable R gene followed the nding that avrBs2
is found in most disease-causing Xanthomonas species
and is required for pathogen tness. The Bs2 NLR gene
from the wild pepper, Capsicum chacoense, was moved
into tomato, where it inhibited pathogen growth. Field
trials demonstrated robust resistance without bactericidal
chemicals. However, rare strains of Xanthomonas overcame Bs2-mediated resistance in pepper by acquisition of
avrBs2 mutations that avoid recognition but retain virulence. Stacking R genes that each recognize a dierent
core eector could delay or prevent adaptation.[1]

5 PLANT BREEDING FOR DISEASE RESISTANCE

5.1.4 Host susceptibility alleles
Most plant pathogens reprogram host gene expression
patterns to directly benet the pathogen. Reprogrammed
genes required for pathogen survival and proliferation
can be thought of as disease-susceptibility genes. Recessive resistance genes are disease-susceptibility candidates. For example, a mutation disabled an Arabidopsis gene encoding pectate lyase (involved in cell
wall degradation), conferring resistance to the powdery
mildew pathogen Golovinomyces cichoracearum. Similarly, the Barley MLO gene and spontaneously mutated
pea and tomato MLO orthologs also confer powdery
mildew resistance.[1]

Lr34 is a gene that provides partial resistance to leaf

and yellow rusts and powdery mildew in wheat. Lr34
encodes an adenosine triphosphate (ATP)binding cassette (ABC) transporter. The dominant allele that provides disease resistance was recently found in cultivated
wheat (not in wild strains) and, like MLO provides broad[1]
More than 50 loci in wheat strains confer disease re- spectrum resistance in barley.
sistance against wheat stem, leaf and yellow stripe rust Natural alleles of host translation elongation initiation
pathogens. The Stem rust 35 (Sr35) NLR gene, cloned factors eif4e and eif4g are also recessive viral-resistance
from a diploid relative of cultivated wheat, Triticum genes. Some have been deployed to control potyviruses
monococcum, provides resistance to wheat rust isolate in barley, rice, tomato, pepper, pea, lettuce and melon.
Ug99. Similarly, Sr33, from the wheat relative Aegilops The discovery prompted a successful mutant screen for
tauschii, encodes a wheat ortholog to barley Mla pow- chemically induced eif4e alleles in tomato.[1]
dery mildewresistance genes. Both genes are unusual
Natural promoter variation can lead to the evolution of
in wheat and its relatives. Combined with the Sr2 gene
recessive disease-resistance alleles. For example, the rethat acts additively with at least Sr33, they could provide
cessive resistance gene xa13 in rice is an allele of Os-8N3.
durable disease resistance to Ug99 and its derivatives.[1]
Os-8N3 is transcriptionally activated byXanthomonas
oryzae pv. oryzae strains that express the TAL eector
PthXo1. The xa13 gene has a mutated eector-binding
5.1.3 Executor genes
element in its promoter that eliminates PthXo1 binding
and renders these lines resistant to strains that rely on
Another class of plant disease resistance genes opens PthXo1. This nding also demonstrated that Os-8N3 is
a trap door that quickly kills invaded cells, stopping required for susceptibility.[1]
pathogen proliferation. Xanthomonas and Ralstonia
Xa13/Os-8N3 is required for pollen development, showtranscription activatorlike (TAL) eectors are DNAing that such mutant alleles can be problematic should the
binding proteins that activate host gene expression to endisease-susceptibility phenotype alter function in other
hance pathogen virulence. Both the rice and pepper linprocesses. However, mutations in the Os11N3 (OsSeages independently evolved TAL-eector binding sites
WEET14) TAL eectorbinding element were made by
that instead act as an executioner that induces hypersenfusing TAL eectors to nucleases (TALENs). Genomesitive host cell death when up-regulated. Xa27 from rice
edited rice plants with altered Os11N3 binding sites reand Bs3 and Bs4c from pepper, are such executor (or
mained resistant to Xanthomonas oryzae pv. oryzae, but
executioner) genes that encode non-homologous plant
still provided normal development function.[1]
proteins of unknown function. Executor genes are expressed only in the presence of a specic TAL eector.[1]
Engineered executor genes were demonstrated by successfully redesigning the pepper Bs3 promoter to contain two additional binding sites for TAL eectors from
disparate pathogen strains. Subsequently, an engineered
executor gene was deployed in rice by adding ve TAL
eector binding sites to the Xa27 promoter. The
synthetic Xa27 construct conferred resistance against
Xanthomonas bacterial blight and bacterial leaf streak
species.[1]

5.1.5 Gene silencing

RNA silencing-based resistance is a powerful tool for engineering resistant crops. The advantage of RNAi as a
novel gene therapy against fungal, viral and bacterial infection in plants lies in the fact that it regulates gene expression via messenger RNA degradation, translation repression and chromatin remodelling through small noncoding RNAs. Mechanistically, the silencing processes

7
are guided by processing products of the double-stranded
RNA (dsRNA) trigger, which are known as small interfering RNAs and microRNAs.[27]

8 See also
Disease resistance in fruit and vegetables
Gene-for-gene relationship

Host range

See also: Plant pathology

Plant defense against herbivory

Plant pathology
Plant use of endophytic fungi in defense

Among the thousands of species of plant pathogenic mi Systemic acquired resistance

croorganisms, only a small minority have the capacity to
Sainsbury Laboratory
infect a broad range of plant species. Most pathogens instead exhibit a high degree of host-specicity. Non-host
plant species are often said to express non-host resistance.
The term host resistance is used when a pathogen species 9 References
can be pathogenic on the host species but certain strains
of that plant species resist certain strains of the pathogen
9.1 Notes
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Epidemics and population biology

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 of plant-pathogen coevolution. Hence as long
as novel pathogens are not introduced/do not evolve, such
populations generally exhibit only a low incidence of severe disease epidemics.[28]
Monocrop agricultural systems provide an ideal environment for pathogen evolution, because they oer a
high density of target specimens with similar/identical
genotypes.[28]
The rise in mobility stemming from modern transportation systems provides pathogens with access to more potential targets.[28]
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.[28]

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[17] Sadanandom, Ari; Bailey, Mark; Ewan, Richard; Lee,
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New Phytologist 196 (1): 1328. doi:10.1111/j.14698137.2012.04266.x. PMID 22897362.
[18] Trujillo, M; Shirasu, K (August 2010). Ubiquitination
in plant immunity.. Current Opinion in Plant Biology
13 (4): 4028. doi:10.1016/j.pbi.2010.04.002. PMID
20471305.
[19] Craig, A.; Ewan, R.; Mesmar, J.; Gudipati, V.; Sadanandom, A. (10 March 2009). E3 ubiquitin ligases and plant
innate immunity. Journal of Experimental Botany 60 (4):
11231132. doi:10.1093/jxb/erp059. PMID 19276192.
[20] Moon, J. (1 December 2004).
The UbiquitinProteasome Pathway and Plant Development.
The Plant Cell Online 16 (12):
31813195.
doi:10.1105/tpc.104.161220.
[21] Trujillo, Marco; Shirasu, Ken (1 August 2010). Ubiquitination in plant immunity. Current Opinion in Plant Biology 13 (4): 402408. doi:10.1016/j.pbi.2010.04.002.
PMID 20471305.
[22] Shirsekar, Gautam; Dai, Liangying; Hu, Yajun; Wang,
Xuejun; Zeng, Lirong; Wang, Guo-Liang; Hu, Yajun;
Wang, Xuejun; Zeng, Lirong; Wang, Guo-Liang (2010).
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.

10

EXTERNAL LINKS

[23] Ting, J. P.; Willingham, S. B.; Bergstralh, D. T.

(2008). NLRs at the intersection of cell death and immunity. Nature Reviews Immunology 8 (5): 3729.
doi:10.1038/nri2296. PMID 18362948.
[24] Tabashnik, Bruce E.; Brevault, Thierry; Carriere, Yves
(2013). Insect resistance to Bt crops: lessons from the
rst billion acres. Nature Biotechnology 31: 510521.
doi:10.1038/nbt.2597.
[25] Kaniewski, Wojciech K.; Thomas, Peter E. (2004). The
Potato Story. AgBioForum 7 (1&2): 4146.
[26] Lacombe et al., 2010 Interfamily transfer of a plant
pattern-recognition receptor confers broad-spectrum bacterial resistance, Nature Biotech 28, 365369
[27] Karthikeyan, A.; Deivamani, M.; Shobhana, V. G.;
Sudha, M.; Anandhan, T. (2013). RNA interference:
Evolutions and applications in plant disease management. Archives of Phytopathology and Plant Protection
46 (12): 1430. doi:10.1080/03235408.2013.769315.
[28] McDonald, B. A.; Linde, C (2002). Pathogen population genetics, evolutionary potential, and durable resistance. Annual Review of Phytopathology 40: 34979.
doi:10.1146/annurev.phyto.40.120501.101443. PMID
12147764.

9.2 Further reading

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 plantpathogen interactions. Nature Reviews Genetics 11: 539.
doi:10.1038/nrg2812.
Schumann, G. Plant Diseases: Their Biology and
Social Impact. 1991 APS Press, St. Paul, MN ISBN
0890541167

10 External links
http://www.apsnet.org/

11
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