Plant immunity Flashcards
Challenges for plants when surviving pathogens
- they are sessile
- They have no adaptive immunity (No somatic recombinatino of immunogobulin genes to encode antibodies)
- No mobile immune cells/ organs (lymphocytes)
PLant immunity consists of:
- Two tired Innate immunity -> (active responses: PTI and ETI, induced responses)
- Pre-existing barriers (passive)
- Cell-autonomous immune system (present in every plant cell in the plant)
Pre-existing barriers
Physical barrier
- Bark
- Cuticle + cell wall
- Elevated stomata – harder to enter
Chemical barriers
- eg. tomatine in tomatoes (BUT pathogens can make enzymes to cleave toxin)
Chemical (phytotoxin) insesitivity
- e.g. maize Hm1 encodes reductase enzyme that reduces HC-toxin of fungal maize leaf spot pathogen
Plant doesn’t provide essential nutrients to pathogen
Pathogen doesn’t recognise host
Organ specific Induced responses
Stomatal closure
- pre-invasive immunity as stomatal cells sense pathogens + close
- (P. syringae makes coronatine phytotoxin which re-opens stomata)
Tylose formation in xylem
- tylose = outgrowths of xylem parenchyma cells into lumen of vessels → blocks vessel + prevents pathogen spread
Leaf abscission
- excise infected area from leaf / lose whole leaf
- E.g. Cherry shot hole on cherry leaf
Cork formation
- suberin waxy hydrophobic layer lines infected site to prevent further entry / spread of pathogen
- e.g. Potatoes challenged by pathogen
induced cellular responses
ROS/Oxidative burst
- reactive oxygen species damage pathogen, signal locally, (in)activate proteins, crosslinks cell walls
apoplastic ROS burst
Hypersensitive response HR
- rapid death of cells restricts pathogen growth -> Programmed cell death
- Stops biotrophs?
- e.g. Infection of resistant tomato byCladosporium fulvum(fungus)
Extracellular traps
- secreted DNA = trap for microbes
- e.g. R. solanacearum on pea escapes trap by secreting nucleases
Callose deposition
- extracellular deposition of callose -> Local, focal strengthening of cell wall
- Response to fungal attempts to penetrate cell wall via appressorium
PR protein accumulation
- pathogenesis related proteins accumulate in apoplast + vacuole at high levels upon infection due to signalling
- V diverse proteins -> many hydrolytic + damage pathogen directly
Phytoalexin accumulation
- Broad spectrum of antibmicrobial activities
- Type of phytoalexin is species specific – pathogen adapts to evade ones specific to host species
Temporal vs spatial immune responses
LOCAL response:
Minutes/hours:
- Protein phosphorylationcascades
- ROS burst (Reactive Oxygen species)
- Ion fluxes inside the cell
E.g. calcium influx inside the cell is important for signaling to proteins in the cell.
Hours/days:
- Transcriptional reprogramming (gene expression is geared towards combating the pathogen threat)
- Hormone biosynthesis (SA, JA, ET) -> used for signaling
- Hypersensitive Response (HR, PCD)-> Programmed cell death
Days:
- Callose deposition
- PR proteins Encoded by genes prodiced within a few hours.
- Phytoalexin production
Systemic response: Induced responses in more distant tissues
- Induced
- Broad range
- Costly (stunt growth)
- Adaptive
- Controlled by salicylic acid signalling (SA)
Leads to System aqcuired resistance as plant carries out these mechanisms protecting from future infection -> however, mechanisms are costly
Strategies to increase crop resistance
Crop can promotes immunity to future infection via SA release (important regulator of SAR)
Can induce immunity using SA analogue
E.g. Actigard/BION (Syngenta) mimics SAso if plants are sprayed, they become temporarily more resistant
-> reduces growth as plant induces immune response where there will be no threat from pathogen -> expensive
1) Induce one immune responseperminantly
- usually unsuccessful
2) Constitutive immune responseperminantly
- Successful but high SA level -> reduces growth
Instead it is more effective for plants to prime PRR and NLR for infection
Pathogen recognition: PAMP triggered immunity (PTI)
- PAMPs recognised by PRR on cell surface
- Universal immune response through PTI
Host -> No disease
PTI & ETI induce responses like ROS burst, callose, PR proteins, phytoalexins, (HR only in ETI)
PTI supression: Effector triggered susceptibility (ETS)
- Specialised pathogens make effectors (eg. inhibitors / enzymes)
- Effectors encoded by AVR genes
- Effectors delivered into host cell via T3SS (by bacteria) or haustorium (by fungi / oomycetes)
- Effectors block PTI signalling
Host = susceptible → compatible interaction where plant supports pathogen
Pathogen recognition: Effector triggered immunity (ETI)
- Specialised pathogen effector recognised by immune receptors (e.g. Nod-Like Receptors) leading to ETI
- Response = universal + often includes hypersensitive response (PCD -> not with PTI)
- Avr gene in one pathogen would trigger effective resistance when expressed by another pathogen
Host = resistant → incompatibility interaction – plant does NOT support pathogen
Host vs non- host interactions
Non-host: plant can repel pathogen
host: plant cannot repel pathogen
Type-I non host: Pathogen triggers PRR -> PTI response
Host: pathogen produces effectors to block PTI signalling -> infection
Type-II non host: Pathogen produces effectors to block PTI signalling, but host recognises the effectors -> ETI response
PTI: PAMPs and PRR
Pathogen-associated Molecular Patterns (PAMPs)
- e.g. flagellum
Pattern Recognition Receptors (PRRs)
- PRRS can be transferred from species to species to allow resistance
- e.g. Tomato senses flagellum but cannot sense bacterial PAMP EF-Tu -> can be moved from Arabidopsis to the tomato leading to broad-range bacterial resistance!
ETI: NLRs
> 70% of the cloned R genes encode NLR (NB-LRR) proteins
NLRs:
- HIghly polymorphic and confer resistance to pathogenss (by recognising effectors)
- Nucleotide binding region: ADP bound when inactive, ATP when active
- Leucine-rich-repeat: protein-protein binding region (trigger)
Direct activation
- Effector binds -> ADP-ATP -> oligomerisation into resistosomes -> Create pore in cell membrane -> Ca+ influx and cell death
Indirect activation
Guard model
- NLR guards host target and is sensitive to its broken down products
- e.g. RPS5 guards PBS1 (host kinase) which is broken down by AvrPphB (from bacteria) -> Cleaved PBS1 activated RPS5
Decoy model
- Host creates a decoy for effector to break down, which is guarded by the NLR
- e.g. PBS1 mimics BIK1 (intended AvrPphB target). AvrPphB breaks down PBS1 by mistake, activating RPS5
Integrate decoy model
- Decoys can be integrated into the NLR proteins (rather than NLR guarding)
- e.g. PopP2 (effector) inactivatates expression of WRKY (TF regulating defence gene expression). WRKY integrated into NLR -> when expression inactivated -> ETI response
Consequences of Indirect activation
Some R genes (NLRs) having dual recognition (e.g. if pathogens target same host protein leading to same product to detect)
Plants have less R genes (NLRs) than pathogens (100 R genes vs 10,000 pathogens)
More durable – as only way to evade indirect recognition is by stopping the manipulation of host target which has a virulence penalty (less virulent)
Limits to transfer of R genes (NLRs) as specific to protein found in that plant
R genes in agriculture
Boom and bust cycles
- Cycle as resistant strains are developed, R genes are fixed then resistant pathogens evolve
- Single R genes = NOT durable → get arms race as R genes fixed by selective sweeps (artificial selection) in agricultural cultivars and then get new pathogen strain (strong selective pressure) and then new R gene so on…
In nature
- R genes NOT fixed and diversity is maintained at the population level -> R genes under balancing selection -> R gene frequency depends on pathogen pressure which decreases once most individuals are resistant so not fixed -> cost to maintaining R gene if pathogen not present
- R genes are present that are thousands of years old
Durable crop rotation
R gene rotation (pathogen dependent) – crop rotation w/ different resistance genes -> stop pathogen being able to evolve new mechanisms
Polycultures – indivs identical except for R gene -> reduce selection pressure on pathogen
R gene stacking – stack R genes in cluster so one crop recognises many proteins of same pathogen -> hard for pathogen to evade to all mechanis -> remember that R genes come at a cost
More R genes are required
- Recruit from larger germplasm (cross-species/taxons)
- Look into wild relatives
- (Synthetic) R genes for crucial ‘core’ effectors
