Plant Immunity and Plant Defense

structural defense barriers

insoluble polymeric structures that are difficult for the pathogen to penetrate

Biochemical defense mechanisms

operate via lipid or water soluble small to medium size molecules or macromolecules like proteins and RNA. The molecules are toxic to pathogen, and weaken pathogen structures like cell walls or inhibit pathogen virulence factors

nonhost resistance

plant remains healthy because the pathogen is not adapted to affect that plant. majority of plant-pathogen interactions

quantitative resistance

impacts severeness of disease symptoms. pathogen is adapted to the plant species and not recognized by major R-gene product. high QR = mild or late disease development, and low QR = severe or early disease development. mostly pathogen race non-specific

monogenic resistance

R-gene mediated resistance. acts on adapted pathogens. plants stay healthy if they express major R-gene that matches race-specific Avr gene of pathogen

QTL

quantitative trait loci. each of several loci that contribute to resistance phenotype in race-nonspecific resistance

divided into major and minor QTL depending on contribution to overall resistance

is major QTL the same as major R genes?

no

R gene

corresponds to one gene in pathogen race to be efficient in activating defense

usually encodes receptor protein that directly or indirectly recognizes avirulence factor / effector, triggers ETI

ETI turns virulence function of effector to an avirulence function (Avr gene), leads to complete host resistance

what can explain absence of disease if a pathogen is present?

surface cells lack recognition factors that can be recognized by pathogen

plant may nor provide some of the substances essential for the survival, development or infection of a pathogen (plant is resistant)

host does not have receptors or sensitive sites for pathogen toxins (usually fungus) or effectors

secondary metabolites

derived from compounds of primary metabolism, not essential for basic plant growth and development

examples of secondary metabolites

tannins, coumarins, quinones, flavonoids, waxes, polyketides, terpenes, alkaloids, cyanogenic glycosides, glucosinolates

phenolics

a group of aromatic compounds or aromatic derivatives

many secondary metabolites are phenolics

proinhibitins/inhibitins

also called phytoanticipins

constitutively synthesized in nonstressed situations (absence of pathogen), stored in plant cell vacuole in inactive glycosylated form

helps plants resist certain pathogenic of phytoanticipin accumulation inside plant or being released onto outside of plant or into soil

phytoanticipin classes: phenolics, tannins, fatty acid-like compounds, coumarins, saponins

postinhibitins

also called phytoalexins

synthesized “de novo” upon infection with pathogen, UV light stress or wounds

a-tomatine

phytoanticipin in tomatoes and related plants

protects against many pathogen strains including Septoria lycopersici

to infect the plant, pathogen must produce tomatinase that detoxifies a-tomatine

antimicrobial peptides (AMPs)

varied, can be found in all plant organs, different antimicrobial activities, can be synthesized constitutively or upon contact with pathogen

some are very small but structurally complex (barrel and b-sheet structures, disulfide bridges)

CPPs

cell-penetrating peptides, type of AMP

can translocate across pathogen membrane or transfer bioactive cargos into pathogen cytoplasm

plant lectins

display antifungal, antibacterial or antiprotozoal activity

bind to carbohydrates on cell wall or membrane

interfere with biofilm formation

reduction in virulence or cause pathogen lysis

concanavalin A, BanLac, Helja

elicitor

pathogen signals that trigger plant defense reactions

exogenous or endogenous

requires receptor proteins on plant side to activate defense

exogenous elicitor

derived from pathogen

microbe or pathogen associated molecular patterns (MAMPs or PAMPs) → pathogen trigger immunity

effectors → effector triggered immunity

endogenous elicitor

derived from plant

damage associated molecular patterns (DAMPs) → pathogen triggered immunity

molecules of intracellular host metabolism released when plasma membrane disintegrates due to pathogens

endogenous peptide elicitors produced in controlled matter

volatile organic compounds

what are peptide elicitors made of?

LRR repeats, kinase domain

what are exogenous carbohydrate elicitors made of?

LysM domain, kinase domain

what are cell surface R-proteins made of?

exterior N-terminal domain LRR (oligomerization, signalling)

central domain TMD (nucleotide binding, regulation)

internal C-terminal domain KD (specificity, regulation)

associated resistance mechanisms

genes that influence interaction outcome other than classic receptor genes

encode proteins that detoxify pathogen effectors, can be underlying major QTL

unconventional R proteins, susceptibility factors (genes), promoter decoys

steps of pattern triggered immunity

1. recognition of PAMPs by pathogen recognition receptors (PRRs) at cell surface induce signaling events

2. transphosphorylation events by receptor-like kinases (RLKs) used for rapid ion flux of Ca2+ into cytosol

3. activation of RBOHD NADPH oxidase produces ROS in apoplast

4. activation of mitogen-activated protein kinase (MAPK) cascades, Ca2+ dependent protein kinases (CDPKs) convey immune signal to nucleus via transcription factor activation

5. transcription activation of PTI genes

effector triggered immunity

mostly hypersensitive reaction (programmed cell death)

directly interact with effectors, interact with effector targets, interact with decoy proteins that act as molecular trap for effectors

direct interaction btwn effector and R protein mediated by integrated decoy protein domain that became part of R protein during evolution

cell wall-associated defenses

morphological change in cell wall or changes derived from wall being invaded by pathogen

1. outer layeer of parenchyma cells produces amophous fibrillar material, traps incompatible bacteria, prevents it from multiplying

2. cell walls thicken by producing cellulosic material infused with phenolic substances, cross-linked to increase resistance

3. callosic papillae/cell wall appositions deposited inside cell walls in response to invasion by filamentous pathogens

histological defense structures

1. formation of cork layers: infection by pathogen induces plants to form several cork cell layers beyond point of infection

2. formation of abscission layers: formed on young active leaves of stone fruit trees. gap formed between two circular layers of leaf cells surrounding locus of infection

3. formation of tyloses: overgrowths of protoplast that protrude into dead xylem vessels through pits, clogging vessels completely

4. deposition of gums: deposited into intercellular space and within cells surrounding infection locus. forms impenetrable barrier that encloses pathogen and isolates it

5. necrotic structural defense reaction: barrier to insulate biotrophic and hemibiotrophic pathogens from healthy tissue (hypersensitive reaction)

induced biochemical defenses

1. production of reactive oxygen species (ROS): hallmark of plant pathogen interaction. most common are O2-, H2O2, and OH

2. pathogenesis-related proteins: structurally diverse, more strongly or exclusively expressed duting plant-pathogen interaction. toxic to fungal pathogens or directly inhibit pathogen functions. Families PR-1 to PR-17

common hormones in plant immunity and defense reactions

abscisic acid (ABA), salicylic acid (SA), jasmonate (JA), ethylene (ET)

SA defends against biotrophic and hemibiotrophic pathogens

JA/ET defend against hemibiotrophic and necrotrophic pathogens

what does it mean that ABA-, SA- and JA/ET signalling is partially antagonistic?

SA-mediated responses can suppress JA/ET response and vice versa

plant immunization

pre-exposed naive plants can show earlier response and stronger resistance to microbes

can act locally (response restricted to same organ as innoculation) or act systemically (protection spreads to all plant organs)

systemic acquired resistance (SAR)

induced by local leaf infection of avirulent pathogen, treatment of unspecific elicitors or with Avr-effectors

protects against biotrophic and hemibiotrophic pathogens

salicyclic acid (SA), pipecolic acid (Pip)

pathogenesis related genes locally and systemically expressed

induced systemic resistance (ISR)

takes place between root and shoot

inducers: plant growth promoting rhizobacteria or plant growth promoting fungi in rhizosphere, live as root endophytes

protects systemic root and shoot tissue against hemibio and necrotrophic pathogens

depends on JA/ET