NLR-Mediated Plant Immunity Flashcards
What do NLRs trigger upon recognition of an adapted pathogen?
Hypersensitive response.
What is recognised by NLRs?
Cytoplasmic pathogen effectors that have been released by the haustorium or by a bacterium.
How does the hypersensitive response protect the plant from infection?
Programmed cell death of infected cells kills the pathogen, and the rest of the plant tissue is saved from infection.
How do NLRs mediate programmed cell death?
It is not yet understood.
Give the 3 classical NLR domains.
- N-terminal Coiled-Coiled or TIR domain
- Central nucleotide binding pocket (NB-ARC)
- LRR domain
Give the roles of the CC/TIR domain.
Signal transduction, protein/protein interactions, execution of cell death.
Give the roles of the NB-ARC domain.
Mediates large conformational changes to regulate activity of NLR, nucleotide binding domain and has been suggested that it also drives receptor oligomerisation.
Give the roles of LRR domain.
Effector recognition, role in auto-inhibition.
How are the levels of NLR protein and mRNA kept low? Why is this needed?
- NLRs are constantly ubiquitinated and degraded by the proteasome.
- Necessary to prevent unwanted host cell death.
How is the folding of NLRs tightly regulated?
By specialised chaperone proteins that ensure NLRs fold correctly and remain inactive.
Describe the inactive conformation of NLRs.
The LRR domain interacts with the ARC domain, keeping the structure in a closed conformation.
How does the NLR form the active conformation upon effector recognition?
Effector binds LRR, releasing it from the ARC domain to give a more open conformation. ARC domain can now bind ATP (replaces ADP) to give the active form of the NLR.
What happens to effectors that are secreted into plant cells?
Either bound by NLRs, or enable the pathogen to colonise the plant if the plant does not express a receptor for that effector.
Describe race-specific resistance.
If some plants express a receptor against an effector from a particular pathogen strain, those plants have race-specific resistance.
Describe broad-spectrum resistance.
If an effector is conserved between multiple pathogen races and the plant expresses a receptor against the effector, the plant has broad-spectrum resistance to pathogens that secrete that effector.
Can expression of multiple R gene receptors be used to give broad spectrum resistance to crops?
No, this reduces plant fitness and reduces the total seed number. A reduction in plant fitness results in increased susceptibility to infection.
Give the two methods of effector detection by NLRs.
- through direct binding
- through NLR recognition of a conformational change in a host protein caused by effector binding (indirect)
What is the guard hypothesis?
R proteins indirectly recognise pathogen effectors by monitoring the integrity of host cellular targets.
Give an example of an effector that is recognised indirectly by an NLR.
AvrPphB - from Pseudomonas syringae.
- binds RPS5 which allows RPS5 to cleave PBS1
- PBS1 cleavage is recognised by the NLR
Why have some NLRs evolved to have additional integrated domains?
Thought to have evolved from effector targets to mediate pathogen detection, either by binding effectors or acting as substrates for effector activity - allows misdirecting of effectors to NLRs instead of essential plant proteins.
Give an example of NLRs working in pairs, where the NLRs have integrated domains.
Rice blast - M. oryzae.
- RGA5 and Pik1 in rice plants have HMA integrated domains.
- HMA was originally a susceptibility factor and was targeted by the Avr-PikD effector.
- Pik1 sensor NLR binds Avr-PIkD via the HMA domain
- Sensed by Pik2 helper NLR
Why would a plant carry a susceptibility factor in its genome?
It is essential for other growth processes - pathogen effectors exploit this and target plant essential proteins
Why do paired NLRs tend to be found back to back within the plant genome?
Allows coordination of their expression.
Give examples of NLR pairs found back to back in the genome.
Pik1/Pik2
RGA4/RGA5
