plant growth and cell signalling: immune response Flashcards
Strategies of pathogenicity
- Necrotrophs kill cells and then consume the contents
- Biotrophs live within host tissue without causing death (need living host)
- Hemibiotrophs firstly depend on living tissue but eventually switch to an necrotrophic lifestyle and kill tissue for further colonisation
Virulent and avirulent pathogens
- A virulent pathogen is one that a plant has little specific defense against
- An avirulent pathogen is one that may harm but not kill the host plant
Plants have chemical and physical defences to pathogens
physical e.g. leaf cuticle and cell walls
chemical e.g. antimicrobials
- Plants are ‘sitting targets’ for pathogens
- They have a strong first line of defence in the cuticle
- However wounds in the cuticle or stomatal openings allow in pathogens
- Plants produce far more secondary metabolites than other kingdoms, including anti-microbial chemicals – chemicals that work well are therefore selected for
What factors influence the plant-pathogen relationship?
Plants are exposed to countless microbes, but very, very few of these interactions lead to disease.
Why?
The disease triangle:
Host-Pathogen-Environment
- The host plant must be susceptible to the pathogen
- The pathogen must be able to overcome plant defenses
- The environment must tip the balance in favor of the pathogen
Response varies according to the time of day/ year
– microbial pathogens tend to attack early in the morning when conditions are damp and guard cells open
-herbivory occurs more during the middle of the day
^the plant responds accordingly)
Molecular interplay between host plant cell and pathogen
A pathogen outside plant cell – if there is a receptor for it the inside of the cell responds by producing a resistant response e.g. a chitinase enzyme in response to fungal infection or closing the guard cells to prevent entry
A pathogen inside a plant cell – programmed cell death or amputation of a leaf etc.
- If a pathogen has an effector – such as being able to produce jasmonate this chemical encourages guard cells to open knocking out resistance and allowing entry
- The plant responds by producing specific proteins – if capable of inactivating the effector this provides resistance
The zig-zag model of plant-pathogen interactions
(see diagram)
^The zig-zag model of plant – pathogen interactions
(Adapted from Jones and Dangl (2006) The plant immune system. Nature. 444: 323-329.)
Pathogen is recognized:
Pattern Triggered(Innate) Immunity (PTI)
Pathogen effectors suppress defense response:
Effector Triggered Susceptibility
Defense responses PTI Effector is “recognised”: Effector Triggered(Acquired)Immunity (ETI)
why do plants start off with PTI?
Because ETI requires high energy commitment which is only suitable when under threat therefore adaptive PTI is the best base-level response
PRRs recognise PAMPs (pathogen associated molecular patterns)
How are pathogens recognised?
Pattern recognition receptors (PRRs) detect their PAMPS
Bacterial pathogens and fungal oomycete pathogens outside the cell are recognised by PRRs due to their PAMPS
PAMPS:
PAMPS = Pathogen-associated molecular patterns also known as microbe-associated molecular patterns(MAMPS)
PRRs then initiate defence responses
Many PRRs have:
- an extracellular leucine-rich repeat domain that recognizes conserved microbial elements
- and an intracellular kinase domain
^ they are leucine-rich repeat receptor kinases (LRR-RKs)
only a few PRR/PAMP pairs have been identified so far
Pathogen recognition triggers defence responses
when PAMPS are detected by PRRs:
- this triggers a kinase cascade combined with a calcium ion influx
- leading to a transcriptional response
+ reactive oxygen production
^resulting in a PTI defence response
Pathogens produce effectors that enhance their virulence
Any point between perception and response can be inhibited by microbial effector adaptation disabling proteins in different ways
Microbial effectors suppress the plant immune response and / or contribute to the pathogen’s viability
Defence responses are both local and systemic
Systemic acquired resistance (SAR) involves a mobile signal
A set of generalised defence responses in organs distant from the original site of infection. Triggered by the signal molecule salicylic acid*
In some cases, enhanced resistance is heritable!
*Aspirin increases plants ability to counter infection – a signal that primes against stress – can be used to revive wilted herbs!
Reactive oxygen species move cell to cell contributing to systemic response.
