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