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AI - Plant Immunity > NLR-Mediated Plant Immunity > Flashcards

NLR-Mediated Plant Immunity Flashcards

1
Q

What do NLRs trigger upon recognition of an adapted pathogen?

A

Hypersensitive response.

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2
Q

What is recognised by NLRs?

A

Cytoplasmic pathogen effectors that have been released by the haustorium or by a bacterium.

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3
Q

How does the hypersensitive response protect the plant from infection?

A

Programmed cell death of infected cells kills the pathogen, and the rest of the plant tissue is saved from infection.

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4
Q

How do NLRs mediate programmed cell death?

A

It is not yet understood.

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5
Q

Give the 3 classical NLR domains.

A
  • N-terminal Coiled-Coiled or TIR domain
  • Central nucleotide binding pocket (NB-ARC)
  • LRR domain
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6
Q

Give the roles of the CC/TIR domain.

A

Signal transduction, protein/protein interactions, execution of cell death.

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7
Q

Give the roles of the NB-ARC domain.

A

Mediates large conformational changes to regulate activity of NLR, nucleotide binding domain and has been suggested that it also drives receptor oligomerisation.

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8
Q

Give the roles of LRR domain.

A

Effector recognition, role in auto-inhibition.

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9
Q

How are the levels of NLR protein and mRNA kept low? Why is this needed?

A
  • NLRs are constantly ubiquitinated and degraded by the proteasome.
  • Necessary to prevent unwanted host cell death.
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10
Q

How is the folding of NLRs tightly regulated?

A

By specialised chaperone proteins that ensure NLRs fold correctly and remain inactive.

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11
Q

Describe the inactive conformation of NLRs.

A

The LRR domain interacts with the ARC domain, keeping the structure in a closed conformation.

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12
Q

How does the NLR form the active conformation upon effector recognition?

A

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.

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13
Q

What happens to effectors that are secreted into plant cells?

A

Either bound by NLRs, or enable the pathogen to colonise the plant if the plant does not express a receptor for that effector.

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14
Q

Describe race-specific resistance.

A

If some plants express a receptor against an effector from a particular pathogen strain, those plants have race-specific resistance.

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15
Q

Describe broad-spectrum resistance.

A

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.

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16
Q

Can expression of multiple R gene receptors be used to give broad spectrum resistance to crops?

A

No, this reduces plant fitness and reduces the total seed number. A reduction in plant fitness results in increased susceptibility to infection.

17
Q

Give the two methods of effector detection by NLRs.

A
  • through direct binding

- through NLR recognition of a conformational change in a host protein caused by effector binding (indirect)

18
Q

What is the guard hypothesis?

A

R proteins indirectly recognise pathogen effectors by monitoring the integrity of host cellular targets.

19
Q

Give an example of an effector that is recognised indirectly by an NLR.

A

AvrPphB - from Pseudomonas syringae.

  • binds RPS5 which allows RPS5 to cleave PBS1
  • PBS1 cleavage is recognised by the NLR
20
Q

Why have some NLRs evolved to have additional integrated domains?

A

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.

21
Q

Give an example of NLRs working in pairs, where the NLRs have integrated domains.

A

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
22
Q

Why would a plant carry a susceptibility factor in its genome?

A

It is essential for other growth processes - pathogen effectors exploit this and target plant essential proteins

23
Q

Why do paired NLRs tend to be found back to back within the plant genome?

A

Allows coordination of their expression.

24
Q

Give examples of NLR pairs found back to back in the genome.

A

Pik1/Pik2

RGA4/RGA5

25
Q

What is the role of a sensor NLR?

A

Senses pathogen effectors

26
Q

What is the role of a helper NLR?

A

Is required for sensor NLR activity.

27
Q

Describe negatively regulated NLR pairs.

A

One NLR prevents the activity of the other in the absence of the effector, where effector binding releases the negative regulation.

28
Q

Why must negatively regulated NLR pairs be found in the same region of the genome?

A

If distributed in different parts of the genome, there could be transfer of only the active NLR into another plant during breeding, giving autoactivation and HR.

29
Q

What is hybrid necrosis?

A

Necrosis occurring as a result of breeding plants that encode NLR pairs, or if NLR pairs are mismatched between plants - gives diversification and may account for new plant species.

30
Q

Describe a many-to-one network.

A

Multiple sensor NLRs work with the same helper NLR.

31
Q

Describe a many-to-many network. Give an example.

A

Multiple sensor NLRs work with many helper NLRs in various combinations. Example is the NRC superclade.

32
Q

Describe the NRC superclade.

A

Plants have many sensor NLRs that can recognise effectors from a broad range of pathogens, and these sensor NLRs then converge on multiple NRC helper NLRs, e.g. NRC2, NRC3, NRC4.

33
Q

Describe expansion of helper and sensor NLRs in potato and tomato plants.

A

Expansion across different chromosomes - where 1/3 of NLRs are part of the NRC superclade.

34
Q

What does expansion of NLR networks allow?

A

Recognition of a diverse range of pathogens.

35
Q

How does this expansion occur?

A

Plants duplicate and mutate resistance genes to try and capture new effector proteins that have not been previously encountered.

36
Q

How is the signalling capacity of NLRs maintained during expansion?

A

Helper NLRs evolve more slowly than sensor NLRs to allow maintenance of the downstream signalling pathways.

37
Q

Why can there not be negative regulation in the NRC network?

A

There could be activation of helper NLRs that aren’t paired with sensor NLRs - giving autoimmunity.

38
Q

Why did the NRC superclade evolve?

A

Increases the adaptive landscape of sensor NLRs - more rapid evolution.
Increases robustness of the response, as helper NLRs amplify the signal.
Gives redundancy – signalling can be maintained by other helper NLRs in the network, if one NRC has been suppressed by pathogenic effector protein.

AI - Plant Immunity (3 decks)

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