L8 - Induced Resistance Flashcards
How can plants counter effectors that suppress the initial PAMP triggered immunity
Name and draw the diagram that sums up this behaviour
- Second layer of resistance triggered by effectors
- Called Effector Triggered Immunity (ETI)
- Resistant host genotypes recognise the effectors
- This continual attack and counter attack is sketched in the Z scheme (see slide 6)
How are effectors recognised?
Compare the receptors used to PTI receptors
- Receptors called NLRs used
NLRs differ from PTI receptors (RLKs) in:
- Being intracellular, cytoplasmic for effectors transferred inside cell
- Similar LRR domains but NLRs contain additional domains
Give an example of convergent evolution seen in immune response
- Plant and mammalian immune receptors are very similar!
- Both recognise PAMPs via extracellular receptors
- Both recognise effectors in cytoplasm via NLRs
- In both, recognition triggers oligomerisation of NLRs forming “Resistosome” (plants) and “Imflamasome” (animals)
Is ETI encoded by dominant or recessive resistance genes?
Are the ETI receptors pathogen specific or general?
What is a pathogen strain called if its effectors are recognised by an R gene?
- Dominant R genes
- Different effectors make ETI receptors race specific
- ETI immunity is race-specific resistance
- An avirulent strain
Describe the challenges of race specific resistance
- Effective against some but not all isolates of a pathogen
- R protein can recognise effector = incompatible
- Small mutations in either pathogen effector avirulence genes or host R genes can make incompatible interaction compatible
- Easier to become compatible = weakness in plant defence
Describe the difference between direct vs indirect recognition in ETI receptors
- ETI receptors can interact directly w/ effectors (direct recognition)
- OR the effector has its ‘target’ gene/susceptibility gene and perturbation of this recognised by R protein
- Allows broader recognition as small mutations have less effect
Give an example to demonstrate how small mutations can effect the compatibility between effectors and R proteins when direct recognition is used
Specific recognition of nematode effector RBP1 by R gene Gpa2
- Polymorphism at single site correlated with recognition strength
- Definitive proof from switching P and S in an effector w/ P and vice versa for an effector w/ S ** look in notes
Give an example of indirect recognition
- Rcr3 plant protein guarded by R gene Cf2
- Rcr3 target by fungi, nematodes, oomycetes
- Highlights breadth advantage of indirect recognition + efficient genetic capital
Do NLRs always trigger an immune response alone? Expand on this.
- Not always, some are “paired NLRs”
- “Paired NLRs” have a sensor and a helper, both needed to trigger immunity response
Two mechanisms:
1) Negative regulation model:
- sensor NLR represses auto-activity of helper NLR in absence of pathogen stimuli
- Effector binding to sensor NLR releases suppression
2) Cooperation model:
- sensor + helper NLRs cooperate to induce immune response upon effector binding
- Helper can associate w/ multiple sensors w/ sensors used for specificity - more efficient
List some of the immunity responses post recognition
- Antimicrobial small molecules
- Activation of defence protein genes
- Alterations to cell wall e.g. strengthening
- ROS
- ETI can trigger hypersensitive response (HR) = cell death
- Systematic acquired resistance (SAR)
What is SAR?
How is SAR signalled? Give 4 points of evidence for this
- Systematic acquired resistance (SAR) is broad spectrum disease resistance on non-inoculated leaves
Evidence that salicylic acid (SA) or methylated derivative (MeSA) used in signalling:
1) Application of SA induces disease resistance
2) increased endogenous SA levels precede SAR induction w/ manipulation affecting SAR
3) MeSA levels increase in phloem exudates during SAR
4) SA binding protein SABP2 increase in SAR (required for recieveing signal)
What responses are induced in SAR?
- Expression of “Pathogenesis related (PR) genes/proteins activated in primary + secondary leaves
- Some PRs have antimicrobial properties themselves
- WRKY TFs activated during PTI and ETI which turn on other defense genes
Describe the technique used and evidence given to identify genes required for the SA response
Genetic screen test:
1) PR promoter coupled to a GUS reporter gene
2) Mutants of interest = plants where SA treatment didn’t activate GUS expression
3) Led to identification of master regulator of PR expression NPR1
4) Redox change upon application of SA makes NPR1 dissociate from multimeric structure, move to nucleus + bind TF for PR genes + others
