Plant immunity Flashcards
Highly adapted plant pathogens cause a lot of damage to crops
crops have a natural resistance however plant pathogens produce large numbers of infected particles so rate of random mutations can out maneuver plant resistance.
Most plants are not susceptible to most pathogens.
not many generalist pathogens and if they are they tend to me more likely to be necrotrophic
Plant immunity differs from that of mammals
Our adaptive immune system uses 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
Systemic Acquired Resistance (SAR)
The gene for gene hypothesis
Two scientists working with rust pathogens 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.Phytopathology 32: 653–66).
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
How might this work?
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.
These characteristic elicitor molecules are known in plant pathology as PAMPS or MAMPS (Pathogen or Microbe Associated Molecular Patterns).
…elicits a response.
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.Plant cell to shut down infection as soon as possible.
elicitor and a receptor
There needs to be an elicitor and a receptor in order for there to be resistance.
Plants make a variety of receptors so it makes it harder for pathogens to infect a they have to overcome several different receptors on a plant cell
Pathogens produce effectors
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.
pili to deliver effector proteins into cells.
Nematodes perform a very similar task using stylets as a delivery for effector proteins. They are a group of diverse proteins that have targets within the plant cell. Effector proteins can get in cells to target nucleus/chloroplasts etc.
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)
describe model better
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). these drive things towards high immunity response.
The indirect perception “guard” model
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A Variation on the Zigzag Model to Describe the Evolution of Chitin Signaling in the Interaction between Cladosporium fulvum and Tomato: a continuum of response.
CEBiP is Chitin Oligosaccharide Elicitor Binding Protein
Ecp6 is a C.fulvum effector protein
Cf-Ecp6 is the tomato R gene product
small protein produced by the fungus which will bind chitin and mop this up to stop plants being able to respond to it.
So chitin is a PAMP. fungus will try and block the detection of chitin by its effectors. Effector is being delivered outside the cell and it is being detected outside the cell.
Phytohormones are crucial in pathogen signalling
Plants use phytohormones to signal in response to pathogens
Pathogens have evolved to target phytohormone signalling networks
Defence responses can be “primed” by biotic and abiotic factors
Plants can use their experience of the world around them to anticipate future biotic and abiotic insult
zig zag model of plant immunity
Pathogen-associated molecular patterns (PAMPs): These are molecules, often derived from pathogens like bacteria or fungi, that are recognized by receptors on the surface of plant cells. PAMPs are like alarm bells that alert the plant to the presence of a potential threat.
PAMP-triggered immunity (PTI): When a plant detects PAMPs, it activates a general defense response known as PTI. This response includes various defense mechanisms aimed at stopping the pathogen from invading the plant’s tissues. PTI is like the first line of defense in a plant’s immune system.
Effectors: Pathogens produce effector molecules that they use to manipulate the plant’s immune system and facilitate infection. Effectors can suppress PTI and promote the pathogen’s ability to colonize the plant.
Effector-triggered susceptibility (ETS): This occurs when effectors successfully suppress PTI, rendering the plant susceptible to infection. In other words, the pathogen has disarmed the plant’s initial defense mechanisms and gained the upper hand.
Effector-triggered immunity (ETI): In some cases, plants have specific resistance genes that enable them to recognize the presence of effectors. When a plant detects these effectors, it triggers a more robust and targeted immune response called ETI. ETI is like a specialized defense mechanism tailored to a specific pathogen’s tactics.
Hypersensitive Response (HR): ETI often involves the induction of a hypersensitive response, where the plant deliberately kills its own cells surrounding the infection site. This localized cell death prevents the pathogen from spreading further within the plant.
