Plant Innate Immunity

Question 1

What is plant innate immunity?

Answer 1

A non-specific immune response that plants use to defend against pathogens and environmental stresses
Relies on pre-existing defence mechanisms, rather than learning from a previous infection (like an adaptive immune system)

Question 2

What are the two models of plant innate immunity?

Answer 2

• Spatiotemporal model
• Evolutionary ‘zig zag’ model

Question 3

What is an overview of the spatiotemporal model of plant innate immunity?

Answer 3

• Pre-invasive penetration defence. Before a pathogen enters plant tissue, the plant can trigger defence (e.g. stomatal closure)
• Post-invasive early defence. Local defences usually at the cell wall, such as ROS
• Post-invasive late defence. Hormone-controlled, e.g. JA, SA. Can activate a wide range of defences and long distance defence signals

Question 4

What are ROS and what role do they play in plant innate immunity?

Answer 4

Reactive Oxygen Species
Function as direct antimicrobial molecules and signalling molecules that activate downstream signalling processes

Question 5

What is SA effective against?

Answer 5

• Biotrophic pathogens

Question 6

What is JA effective against?

Answer 6

• Insects (insect damage causes water loss, triggering ABA which works together with JA)
• Necrotrophic pathogens (when produced with ethylene)

Question 7

What happens in the first 0-2 hrs of SA mediated plant immune response?

Answer 7

• Pattern Recognition Receptors (PRRs) on the plant cell membrane detect PAMPs secreted by pathogen
• PRRs activate intracellular signalling cascades, activation of transcription factors
• Transcription factors move to nucleus, induce expression of SA biosynthesis genes

Question 8

What happens in 2-48 hrs of SA mediated plant immune response?

Answer 8

• SA accumulates and alters the cellular redox state
• Redox state causes activation of NPR1 (SA receptor)
• Moves to nucleus
• Activates defence genes

Question 9

What happens 0-10 mins of the JA mediated plant immune response?

Answer 9

• Induced from DAMPs (from cell wall being damaged by herbivores)
• DAMPs recognised by Pattern recognition receptors (PRRs)
• Activated transcription factors which move to the nucleus to activate JA biosynthesis genes

Question 10

What happens 10 min - 3hrs in the JA mediated plant immune response?

Answer 10

• JA and isoleucine act as molecular glue
• Brings COI1 protein in contact with repressor protein JAZ and labels them for degradation
• Meaning JAZ is no longer repressing MYC2
• MYC2 activates defence genes

Question 11

What are glucosinolates?

Answer 11

e.g. in Brassicaceae
- Secondary metabolites
- Function as precursors to a range of compounds that are toxic to herbivores and pathogens
- Plant damage causes glucosinolates to be hydrolysed by myrosinase (from ER / peroxisome)
- Releases compounds such as toxic mustard oil

Question 12

What are benzoxazinoids?

Answer 12

e.g. in Poaceae
- Plant damage causes benzoxazinoids to be hydrolysed by glucoside hydrolase
- Releases toxic aglycone

Question 13

What is quantitative disease resistance?

Answer 13

• Non host resistance (PTI): very strong and very broadly effective
• Basal resistance (+/- strength, broadly effective)

Question 14

What are the pros and cons of quantitative resistnace?

Answer 14

Pros:
- Very durable, based on multitude of genes and mechanisms
- Broad range of effectiveness

Cons:
- Difficult to select by crop breeders
- Basal resistance is weak and not completely effective

Question 15

What is qualitative resistance?

Answer 15

Race-specific resistance
Based on single resistance genes
e.g. effector-triggered immunity (ETI)

Question 16

What are the pros and cons of qualitative resistance?

Answer 16

Pros:
- Easy to select for by crop breeders
- Very strong resistance

Cons:
- Not durable, based on single R genes, pathogens can evolve a way to breakdown the resistance gene
- Narrow range of effectiveness

Question 17

What do R genes encode?

Answer 17

(Qualitative disease resistance)
- Encode NLR proteins
- NLR: intracellular receptor proteins of virulence factors
- Upon activation, NLRs induce a hypersensitive cell death response (HR)

Question 18

What is the zig-zag model of plant innate immunity?

Answer 18

1. PAMP-triggered immuntiy (PTI)
   - Plants detect PAMPs using PRRs, initiating PTI
2. Effector-triggered susceptibility (ETS)
   - Pathogens secrete effectors (virulence factors) to interfere with PTI, plant more susceptible to infection
3. Effector-triggered immunity (ETI)
   - Plants recognise these effectors, often through R genes and NLRs, triggering a stronger more rapid immune response, leading to hypersensitive cell death (HR)
4. Evolution of pathogens and plants
   - Pathogens evolve to evade ETI by losing, modifying or acquiring effectors. Plants evolve new R genes to recognise these new effectors, restarting the cycle

Question 19

What is ETI most effective for?

Answer 19

• Cell/phloem feeding insects
• Biotrophic pathogens