Plant immunity Flashcards
What is the difference between plant immunity and mammal immunity?
mammals have adaptive immune systems which use mobile cells and antibodies in detecting and responding to pathogens
Plants have an innate immune system, which combines local responses with systemic signalling to the rest of the plant. Plants also have a long distance mechanism called Systemic Acquired Resistance (SAR) (movement of mobile signals).
Describe the two scientists working with rust pathogens which were responsible for developing the gene for gene model.
R.H. Biffen (1905) showed resistance to be a monogenic trait
H.H. Flor’s experiments (1940s-1950s) on flax AND flax rust (caused by the fungus Melampsora lini) showed that flax resistance genes were dominant, but rust virulence genes were recessive. This led him to propose the gene-for-gene hypothesis (see H.H. Flor (1942) Inheritance of pathogenicity in Melampsora lini.
We now call genes in the pathogen which are involved in overcoming immunity avirulence (Avr) genes
Avr gene products elicit immune responses in plants carrying the corresponding resistance (R) gene
Explain a pathogen in a plant organism
Bacterial cells (and fungi and oomycetes) secrete a lot of waste products, metabolites and gene products, including effectors and those required for heterotrophy.
This results in a signature of characteristic molecules wherever the pathogen is found. Gives its position away in the plant. Plants are really sensitive to chitin in the cell wall of pathogens.
These characteristic elicitor molecules are known in plant pathology as PAMPS or MAMPS (Pathogen or Microbe Associated Molecular Patterns).
Elicits as a response
There is direct recognition. The receptor will bind to the elicitor
once this occurs then there is signalling cascade which may involve Reactive Oxygen Species (ROS), Δ[Ca2+] , protein phosphorylation.
Hypersensitive response
(HR) leading to large biochemical and signalling changes and cell death. This limits movement of pathogens
only resistance if there is the correct receptor for the elicitors
Pathogens produce effectors. What do they do?
Effectors may:
Interfere with plant immunity
Change host metabolism
Make the host a more comfortable place for the pathogen to live
Effectors have a defined target or targets in the plant
Different types of invaders
oomycetes produce haustorium –> then host targets
bacteria–> host targets
nematode gland and stylet help produce –> host targets
A universal model of plant immunity?
The zig-zag model of plant immunity brings together:
Pathogen-associated molecular patterns (PAMPS)
PAMP-triggered immunity (PTI)
Effectors
Effector-triggered susceptibility (ETS)
Effector-triggered Immunity (ETI)
Hypersensitive Response (HR)
Specific classes of receptors are associated with PTI and ETI
PAMP-Triggered Immunity
pattern recognition receptors (PRR) (and BRI1-associated kinase 1 (BAK1))
Effector-Triggered Immunity
Nucleotide-binding leucine-rich repeat (NB-LRR)
How do plants use phytohormones and how have pathogen target this type of signalling?
Plants use phytohormones to signal in response to pathogens
Pathogens have evolved to target phytohormone signalling networks
Why are Salicylate and jasmonate mutually antagonistic?
Perhaps because the pathogenicity of necrotrophs is enhanced by the hypersensitive response, so HR should be suppressed in the presence of necrotrophs.
Give an example of how some pathogens take advantage of the defense signal cross-talk
Pseudomonas syringae producing coronatine which is a mimic of jasmonic acid.
Coronatine is an excellent mimic of JA-Ile, the active jasmonate hormone. By suppressing biotrophic defenses coronatine production significantly enhances the pathogenicity of the bacteria that produce it
Defense pathways intersect with other signaling pathways
Defense responses reduce growth rate. Drought stress and abscisic acid (ABA) accumulation suppresses responses to pathogens.
For necrotroph, jasmonic acid is involved and for biotroph, auxin is involved.
