Week 15 L1: Plant-Microbes pt1 - MICROBE

Question 1

How do bacteria introduce the plant with effectors?

Answer 1

Many bacterial effectors 
are introduced into plant 
cells through Type-III 
secretion systems (T3SS) 
or other secretion 
systems

Question 2

How do fungal and oomycete introduce effectors?

Answer 2

often secreted
from haustoria or
tips of hyphae

Question 3

How do insects introduce effectors?

Answer 3

s introduced via

stylets

Question 4

How do nematodes introduce effectors?

Answer 4

introduced through

the feeding stylet

Question 5

What are the ways effectors act?

Answer 5

1. Bind to the PRR (immune) receptor and inhibit signalling
2. Bind to DNA and turn genes to favour pathogen survival
3. Disrupt chloroplast structure and function.
4. Localise outside plant cells in the apoplast and inhibit the proteases.

Question 6

What is the second layer of defence which is inside the cell?

Answer 6

Resistance proteins (receptors) which recognise and bind R proteins to inhibit their immunosuppression.

Immune response initiated

Question 7

How do the PRR and R proteins differ?

Answer 7

PRR - has an extracellular LRR domain, transmembrane domain and an intracellular kinase domain.

R - LRR, NBS (nucleotide binding domain) and either a CC domain or a TIR domain.

PRR - recognition domain extracellularly

R - cytoplasm

Question 8

Is the PRRs receptor always have an extracellular LRR?

Answer 8

no, it can be another domain

Question 9

What does Flor’s gene-for-gene hypothesis propose?

Answer 9

“For each resistance gene in the host there is a
corresponding gene for avirulence in the pathogen
conferring resistance and vice versa”

So the pathogen needs to have the avirulence gene to be susceptible to resistance gene in plant

Question 10

What is a definition of resistance?

Answer 10

incompatible interaction

Pathogen called avirulent

Question 11

What is a definition of susceptible?

Answer 11

compatible interaction

Pathogen called virulent

Question 12

How do resistance protein recognise effectors?

Answer 12

a) direct

b) guard/decoy

Question 13

How does a decoy recognition work?

Answer 13

The effector bind to proteins in the act of its virulence. The effected protein then is modified and binds to R protein as a act of its avirulence

Indirect recognition of what the effector is doing inside the plant

Question 14

How can the guard proteins minimise the number of specific R proteins needed for a virulence response?

Answer 14

e.g. the Hpa and Psy effectors interact with the same proteins in the cell so the same type of R protein is stimulated.

If we have a pathogens targeting the same proteins then we have an R protein against multiple strains of pathogens

Question 15

What happens if a host does not have a specific R protein for the pathogen?

Answer 15

increased pathogen fitness

Question 16

What does the effector trigger when it binds to proteins in the cell?

Answer 16

triggers favourable transcription

nutrient production

Question 17

Can a R protein only recognising 1 of protein-effector interaction create resistance?

Answer 17

YES, immunity is triggered, only takes 1 recognition by the R protein

Question 18

What is a decoy model?

Answer 18

The plant has decoy targets, the protein is beneficial for disease. effector targeting this protein will have no benefit.

Evolved its protein to be able to bind to effector protein.

But the effector protein can still target it to trigger immunity.

Question 19

What does stimulation of R proteins lead to? (5)

Answer 19

Activated R proteins signal danger, and trigger a
heightened defence response that includes:

• Production of the stress hormone salicylic acid (SA)
• Production of reactive oxygen species (ROS)
• The hypersensitive cell death response (HR)
• Expression of pathogenesis-related (PR) proteins
• Systemic signals and systemic acquired resistance
(SAR)

Question 20

What immunity is simulated in R proteins?

Answer 20

ETI

Enhancer Triggered Immunity

Question 21

What is the process of SAR - Systemic Acquired Response?

Answer 21

1. Binding of pathogen to plasma membrane induces a signal transduction pathway.
2. The STP causes hypersensitive response (HR), which kills infected plant cells, before they die they release antimicrobial molecules.
3. Dying cells release SA which is transported throughout the plant.
4. In healthy cells throughout the plant, SA induces a STP that produces antimicrobial molecules. PREVENTING FURTHER INFECTION.

Question 22

How do we improve resistance? Molecular approach

Answer 22

Paradigm shift for resistance.

Screen for essential pathogen effectors and select for these R genes in resistant crops.

Can KO essential effector in the pathogen.

Can pick the right resistance gene or even modify it.

Question 23

How do we improve resistance? Biotechnological approaches

Answer 23

Approaches to prevent ETS:
• Breeding to select for natural variants of targets that can not interact with effectors
• Synthesize host targets (gene editing) that can not interact with effectors

Can we engineer a potato with mutation from StVPS52 which will not interact with barleys aphid pathogen Rp1.

NO host response.

Question 24

Is there a specificity in the plant microbe interaction?

Answer 24

YES
e.g. Mp1 (APHID) interaction with AtVPS52 protein of potato

But the aphid cannot target barleys protein.