Week 15 L1: Plant-Microbes pt1 - MICROBE Flashcards
How do bacteria introduce the plant with effectors?
Many bacterial effectors are introduced into plant cells through Type-III secretion systems (T3SS) or other secretion systems
How do fungal and oomycete introduce effectors?
often secreted
from haustoria or
tips of hyphae
How do insects introduce effectors?
s introduced via
stylets
How do nematodes introduce effectors?
introduced through
the feeding stylet
What are the ways effectors act?
- Bind to the PRR (immune) receptor and inhibit signalling
- Bind to DNA and turn genes to favour pathogen survival
- Disrupt chloroplast structure and function.
- Localise outside plant cells in the apoplast and inhibit the proteases.
What is the second layer of defence which is inside the cell?
Resistance proteins (receptors) which recognise and bind R proteins to inhibit their immunosuppression.
Immune response initiated
How do the PRR and R proteins differ?
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
Is the PRRs receptor always have an extracellular LRR?
no, it can be another domain
What does Flor’s gene-for-gene hypothesis propose?
“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
What is a definition of resistance?
incompatible interaction
Pathogen called avirulent
What is a definition of susceptible?
compatible interaction
Pathogen called virulent
How do resistance protein recognise effectors?
a) direct
b) guard/decoy
How does a decoy recognition work?
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
How can the guard proteins minimise the number of specific R proteins needed for a virulence response?
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
What happens if a host does not have a specific R protein for the pathogen?
increased pathogen fitness
What does the effector trigger when it binds to proteins in the cell?
triggers favourable transcription
nutrient production
Can a R protein only recognising 1 of protein-effector interaction create resistance?
YES, immunity is triggered, only takes 1 recognition by the R protein
What is a decoy model?
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.
What does stimulation of R proteins lead to? (5)
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)
What immunity is simulated in R proteins?
ETI
Enhancer Triggered Immunity
What is the process of SAR - Systemic Acquired Response?
- Binding of pathogen to plasma membrane induces a signal transduction pathway.
- The STP causes hypersensitive response (HR), which kills infected plant cells, before they die they release antimicrobial molecules.
- Dying cells release SA which is transported throughout the plant.
- In healthy cells throughout the plant, SA induces a STP that produces antimicrobial molecules. PREVENTING FURTHER INFECTION.
How do we improve resistance? Molecular approach
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.
How do we improve resistance? Biotechnological approaches
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.
Is there a specificity in the plant microbe interaction?
YES
e.g. Mp1 (APHID) interaction with AtVPS52 protein of potato
But the aphid cannot target barleys protein.
