Plant Immunology

1. Plant Immunology:
Definition:
“Plantimmunologyisthe studyof howplantsdefendtheirtissuesfrominfection. Plants do not have an
adaptive immune system, but have evolved innate immune mechanisms to sense and respond to
infections.”
Plant Immunity:
Plantimmunityisthe inherentorinducedcapacityof plantstowithstandorward off biological attackby
pathogens. Molecules released from pathogens are recognized by plant cell surface receptors, and
trigger specific signaling that help to defend the plant against attack.
Many plant-associated microbes are pathogens that damage or weaken the plant growth and
reproduction.Plantsrespondtoinfectionusingatwo-branchedinnateimmunesystem. The first branch
recognizesandrespondstomoleculescommontomany classes of microbes, including non-pathogens.
The second responds to pathogen virulence factors, either directly or through their effects on host
targets.
 Pathogenicbacteriaproliferate inintercellularspaces(the apoplast) afterenteringthrough gasor
water pores stomata.
 Nematodes and aphids feed by inserting a stylet. Feeding is accomplished through a hollow,
needlelike mouthpart called a spear or stylet that is directly into a plant cell
 Fungi can directlyenterplantepidermal cells,orextendhyphae on top of, between, or through
plantcells.Pathogenicandsymbiotic fungi can invagination feeding structures (haustoria), into
the host cell plasma membrane.
 Haustorial plasma membranes, the extracellular matrix, and host plasma membranes form an
intimate interface at which the outcome of the interaction is determined. These diverse
pathogenclassesall deliver effector molecules into the plant cell to enhance microbial fitness.
There are two branches of the plant immune system. One uses transmembrane pattern recognition
receptors(PRRs) thatrespondtoslowlyevolvingmicrobial- or pathogen-associated molecular patterns
(MAMPS or PAMPs),suchas flagellin.The secondactslargelyinside the cell, using the polymorphic NB-
LRR protein products encoded by most Resistant genes. They are named after their characteristic
nucleotide binding (NB) and leucine rich repeat (LRR) domains.
Pattern-TriggeredImmunity /PAMP TriggeredImmunity:

2. In nature,plantshave toface pathogenattacks.However,plantdiseasesrarelyoccurdue to efficient
immune systemspossessedbyhostplants.Pathogensare perceivedbytwodifferentrecognition
systemsthatinitiate (patterntriggeredimmunity) PTIand(effector triggeredimmunity)ETI.
Recognitionof Danger Signals:
 Recognitionof dangersignals
 Distinguishself ordamagedself-versusnon-self –fundamentaltoanyimmune system
 PAMP or MAMP – pathogen/microbe-associatedmolecularpattern
 DAMP – damage-associatedmolecularpattern
Uses transmembrane patternrecognitionreceptors(PRRs)
Pattern RecognitionReceptors(receptor-like proteins/kinases)
 Membrane receptors
 Ligand-receptorinteraction
 Initiate signal transductioncascade
 Firstlayerof active defense,extracellularmembranereceptors
 PRRs perceive PAMPsbyreceptor-ligandinteractions
 Evolutionarilyancientandsome widelyoccurringinplantkingdom
 Interfamilytransferof PRRsmore successful thanRgenes
 R proteinsincontrastare evolutionarilyyoung,withmanynovelmembers
ImmunityHormones of Plants:

3.  SalicylicAcid
 JasmonicAcid
 Ethylene
PAMPs:
PAMP recognitionleadstoa chainof signalingevents broadly referred to as general response in plants
and acquiredsystematicresistance.PAMPsare molecularcomponentshighlyconservedwithinaclassof
microbes, where they carry out an essential function for fitness or survival. Plants recognize a wide
range of bacterial PAMPs, most of which are derived from structural components of bacterial cell.
Rarely, some virulent phytopathogenic bacteria are able to mask recognition of a PAMP by mutating
residueswithinrecognizedepitope. This reflects a virulence strategy evolved by successful pathogens
complementary to effector secretions.
Example:
Proteinflagellin,the buildingblockof motilityorganflagellumis recognized by most plants. N terminus
of flagellinactaspotentelicitor.The peptide flg22elicitsresponsesinmostplantspeciesandisasactive
as the full lengthflagellin. Interestingly,the flg22regionisrequired for bacterial virulence and motility,
consistent with the fact that PAMP mutation has a fitness cost for microbes.
Effector Triggered Immunity:
The second tier of Plant Immune System is Effector Triggered Immunity (ETI). This is the type of
immunitythatistriggeredbythe presence of foreigneffectorsinthe cell.Asthe wordsuggestsETIisthe
immunity that occurs in response to the effectors released by pathogens to cause the disease in host.
Although there are certainexceptionsthatviolatethe definitionof ETI Effectortriggered immunity (ETI)
isa propertyof the innate immune system.ETIwasfirstidentifiedinplantsbuthas also been identified
inanimal cells.The innate immune systemis common to all multicellular organisms and forms the first
line of defence against pathogen.
Explanation:
In planinnate immune system,the cellsindividuallyhave the abilitytosense andrespondto a pathogen
attack. The cellsdoso by usingspecificreceptorsthatare knownasNBLRR (Nucleotide BindingsLeucine
Rich Repeats) receptors. The presence of specific pathogen "effectors" activates specific NLR proteins
that limit pathogen proliferation. These effectors are present inside the cells and they detect the
effectorinterference of non-self-pathogens.EffectoractivatedNBLRRreceptorsconnectinvarious ways
in order to transitionally boost the defense mechanism.
The ETI immunity is reliant on R gene that is activated by specific pathogenic strains that invade the
plant cells. Different plant immune systems contain 100-160 different R genes that provide resistance
against various viruses, bacteria, nematodes, oomycetes pathogens and insects. Plant ETI can cause

4. apoptotichypersensitive response. The hypersensitive response (HR) isamechanism used by plants, to
prevent the spread of infection by microbial pathogens.
Effectors:
Effectors typically are proteins that are released outside of pathogens and inside of the host. The
effectorsmanipulate the cell physiologyanddevelopment.Effectorscanalsoevolve frombeing virulent
to beingbeneficial.Forexample,afungal proteinthatfunctionsoutsideof the fungusbutinside of plant
cellshasevolvedtotake on plant-specific functions. Pathogen host range is determined, among other
things,bythe presence of appropriate effectors that allow colonization of a particular host. Pathogen-
derivedeffectorsare apowerful tool toidentifyhostfunctionsthatare importantindisease.Apparently
most effectors function to manipulate host physiology to allow disease to occur. The number of
effectorsapathogenreleasescanaslovary verymuchlike well-studiedbacteriareleasesafew dozensof
effectors while fungi, oomycetes and nematode plant pathogens express a few hundred effectors.
R-Genes and R-Proteins:
R-Genes products contain a broad set of disease resistance responses that can eliminate the invading
pathogenfromspreading and causing the disease. Most of the resistance genes encode for the NBLRR
proteins(leucine richrepeats) orNLR proteins or STAND proteins among other names. The plants have
evolvedR-Genes(Resistance Genes) that allow the recognitions of specific pathogens either by direct
binding to the effectors it releases or by recognizing that the effector is altering the host’s protein. In
this regard it is important to mention:
Guards Hypothesis:Inonlysome cases is there direct interaction between the R gene product and the
Avr gene product.Forexample,bothFLS2andXA21 interactwiththe microbial peptides. In contrast for
the NBLRR class of R genesnodirectinteractionhasbeennoticed.Soa model was according to a model
the R gene interactsorguardsa proteinknownas Guardee which is the target of Avr products. When it
detects the interference with Guardee protein it activates the resistance. This is known as Guards
hypothesis.
Evolution in R-Genes: The R genes have gone through an evolutionary process to combat the virulent
genes(Avrgenes). Asfirstnotedby HaroldFlor inhismid-20thcenturyformulationof the gene-for-gene
relationship,the plantRgene andthe pathogenAvrgene musthave matched specificity for that R gene
to confer resistance, suggesting a receptor/ligand interaction for Avr and R genes. Some Resistance
genesshowstabilityovermillionsof yearseffectiveagainstaspecificpathogenwhilemanyR-Genesthat
occur in small clusters can evolve new pathogen specificities.
Use in Breeding: Plant breeders frequently rely on R genes to obtain useful resistance, although the
durabilityof this resistance can vary by 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
effector gene.
Cell Signaling In Immunity:

5. Cytokinesare secretedbyimmunecellsinresponse tocellularsignaling,andbindto specific membrane
receptors, which then signal the cell via second messengers, often tyrosine kinases, to alter cellular
activity (gene expression)
Perception of Pathogen Presence:
Plantdefense signalingisactivatedbypathogen-detectingreceptors.Theactivatedreceptors frequently
elicit reactive oxygen and nitric oxide production, calcium, potassium and proton ion fluxes, altered
levels of salicylic acid and other hormones. These events in turn typically lead to the modification of
proteins that control gene transcription, and the activation of defense-associated gene expression.
plant defenses can be activated by the sensing of damage-associated compounds (DAMP), such as
portionsof the plant cell wall released during pathogenic infection. Many receptors for, effectors and
DAMPs have been discovered. DAMPs are often detected by transmembrane receptor
Transcription factors and the Hormone Response:
Numerous genes and/or proteins have been identified that mediate plant defense signal.
Cytoskeleton andvesicletraffickingdynamicshelptoorientplantdefense responsestowardthe pointof
pathogen attack.
Mechanisms of Transcription Factors and Hormones:
Plant immune system activity is regulated in part by signaling hormones such as:
1. Salicylic acid
2. Jasmonic acid
3. Ethylene
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-associateddegradationof repressorproteinsthatblockexpressionof certaingenes.
The net result is hormone-activated gene expression.