Lecture 7b: Plant immunity part 2 Flashcards
Disease triangle in depth
Disease can only occur when there is a susceptible host, suitable environment and a pathogen present (disease triangle)
See: http://eagri.org/
Host Factors
a. Occurrence of susceptible varieties in the given locality
b. Developmental stage of the host plant – more commonly infected as juveniles
c. Density and distribution of the host – closely packed plants allows for more disease spread
Pathogen factors
a. Amount of primary (initial) inoculum in the air, soil or planting material
b. Spore germination – conditions required for germination e.g. moisture/heat
d. Infection – virulence factors
f. Sporulation on the infected host
g. Re-dispersal / Dissemination of spores – ability to disperse
h. Perennating stages ?
Environmental factors
a. Temperature – high temp. Promotes
b. Humidity the most influential environmental factor e.g. can be increased when plants are close packed (densely populated) e.g. in rainy season risk is higher
c. Light intensity – low light intensity promotes pathogens – hence less densely packed plants may be more successful
d. Wind velocity
Example of a disease cycle: Life cycle of black stem rust disease
Life cycle of black stem rust disease
(see life cycle diagram in notes)
alt host - barberry supports the pathogen outside the season of wheat plants ‘overwintering’ they can also overwinter on stubble of wheat left in the field
The spores resemble rust on the wheat stem
spore life cycle:
Urediniospores: In Britain, airborne urediniospores generally originate from South West Europe and North Africa. These spores, when air movements are appropriate, cause initial infection on wheat.
Teliospores: Relatively late in the season, black elongated pustules containing the teliospores develop, mainly on the stems. These spores overwinter on wheat stubble.
Basidiospores: Eventually, teliospores produce secondary spores – basidiospores – which infect barberry (Berberisspp.), where the pathogen enters a sexual phase.
Aeciospores: On barberry, aeciospores are produced which can infect crops in close proximity (e.g. wheat close to field edges) very late in the season.
Uredospores: In wheat, infection by aeciospores gives rise to the uredospore stage. This stage is associated with typical symptoms on wheat – orange/brown sporulating pustules, which occur in stripes on leaves and stems.
see video for details:
https://www.youtube.com/watch?v=AeuP5IYP5HA
^Teliospores have a hard coating allowing them to survive harsh winter conditions
When they germinate they form aeciospores that infect barberry plants
- Sexual phase occurs on barberry and spores created
- wind transfers these spores to juvenile wheat plants and infect their stems
Aeciospore Dispersal Model
The model produces projection probabilities to show the density of aeciospores that would likely reach certain distances from an infected Berberis bush under current environmental conditions. This information can then be used to help guide monitoring of Berberis bushes and neighbouring cereal crops for stem rust infection.
How do we model aeciospore dispersal?
A Gaussian Plume Model (GPM) is used here to determine how far aeciospores
would likely travel from a Berberis bush infected with stem rust.
Gaussian Plume Model (GPM)
What are the key factors in the GPM?
1.Source Strength. This is an estimation of the number of aeciospores that could be
released from an infected Berberis bush. These have been approximated at different
intensities of infection based on research at the John Innes Centre.
2.Shape of the Plume. This describes how the ‘cloud of aeciospores’ that are
released from an infected Berberis bush may behave.
What affects the shape of the plume?
The plume shape is dependent on environmental conditions at the given location at
the time of running the model.
This includes:
-Irradiance from the sun.
-Percentage of cloud cover
-Wind speed.
How do these factors affect the shape of the plume?
The plume can be:
1.Unstable. When wind speed is low and Irradiance is high (summer conditions).
2.Neutral. When it is cloudy and wind speed is high.
3.Stable. When the sky is clear and wind speed is low (at night - no solar radiation).
(JIC, Diane Saunders)
Wind speed and dispersal rate can be used to estimate spread of disease
Disease forecasting methods
Forecasting refers to predicting for the occurrence of plant disease in a specified area ahead of time, so that suitable control measures can be undertaken in advance to avoid losses.
Forecasting based on primary inoculums: Assessment of viable spores or propagules in the air assessed by using different air trapping devices.
Forecasting based on weather conditions: Microclimatic condition including parameters like temperature, relative humidity, rainfall, light, wind velocity etc., above the crop and at the soil surface are also recorded.
Forecasting based on correlative information: Weather data of several years are collected and correlated with the intensity of the diseases. Probability based on prev. Years data
Use of technology for disease forecasting - Use of advanced imaging technology for predicting disease incidence
Sensors for crop pest detection
See Mahlein et al 2012
- Low-power Image Sensors – similar to insect traps, collecting spores e.g. on sticky paper among crops
- Acoustic Sensors – used to predict no. Of insects in the field as grasshoppers/bees/wasps emit sound – unusually high no. Of insects could suggest an issue with pests
- Thermography based sensor – higher temp regions of plant suggests infection (image below, top left)
- Fluorescence based sensor - colour change on areas of plant suggests infection (“ “ “ top right)
- Hyperspectral based sensor –multiple wavelengths of light analysed to assess infection (“ “ “ bottom)
- Gas Chromatography based sensor – on infection plants release specific volatiles that can be detected and analysed to assess whether defence response in the plant has been triggered or not
Effective for broadscale field analysis
Integrated pest management (IPM)
Integrated pest management (IPM)
Integrated Pest Management (IPM) is a sustainable approach to managing pests, weeds, and diseases in a farm or food manufacturing facility.
Reducing chemical use for improved environmental health – encouraging natural ecosystem services
Steps for IPM:
*Monitor: Use strategies to track pests, weeds, and diseases
e.g. in the example remove barberry host from surrounding area
*Prevent: Use physical barriers, crop rotation, and other methods to keep pests out
e.g. not growing wheat for consecutive years to prevent disease cycle continuation
*Control: Use a combination of methods, including biological control, plant breeding, and cultural practices
*Reduce reliance on chemicals: Use non-chemical alternatives and only use chemical pesticides as a last resort
Key factors for designing IPM strategy
- Intrinsic Heritable Plant Resistance -Grow more plants that host parasitoids that prey on pests
- Plant Vaccination – administering a low dose of pathogen to provide a heightened immune response to prevent future infection (systemic immunity)
- Inter- and Intra-Specific Botanical Diversity – grow an area of highly susceptible plants to concentrate pest/pathogen on this susceptible variety – capturing them in a small area which can then be cleared/destroyed
- Biorational Synthetic Volatiles – volatiles can trigger immune response without actual infection
- Biological Control –beneficial microorganisms that feed on pathogens
(gov.uk)
see diagram showing how good hygiene – prevents disease spread e.g. clothes or shared machinery
IPM methods
IPM methods
*Crop rotation
*Using trap crops
*Growing pest-resistant varieties
*Practicing good hygiene
*Using physical barriers
*Restricting pests’ access to food, water, and harborage
Benefits of IPM
- Helps manage pesticide resistance
- Minimizes environmental harm
- Supports healthy crops
- Enhances biodiversity and wildlife
- Supports sustainable agricultural production
How can pathogens infect hosts: modes of pathogenesis
Establishment phase (Biotrophy)
Duration: 1-2 days post inoculation
. Mycelia growing parallel to veins
. No cell death
. Lack of ROS
. Cellular integrity intact
Necrotrophic phase (Necrosis)
Duration: Begins at 3days post inoculation
. Mycelia forms infection cushions
. Cell death
. ROS accumulation
. Disintegration of cellular anatomy
^ Biotrophy – surviving within a living host without detection whilst taking nutrients without killing host some pathogens maintain this phase reducing overall host health without killing host
^ Necrotrophic – release molecules that kill the host releasing nutrients that the pathogen takes up to spread further
(not all pathogens have a necrotrophic phase see more in prev lecture)
Extracellular signals in bacteria (PAMPS)
Pathogen Associated Molecular Patterns
PAMPs can be detected by host plants via specialised receptors and are present in all bacteria
PAMPTI – PAMP triggered immunity can occur on detection
List of bacterial PAMPS
List of bacterial PAMPS:
Teichoic and lipotechoic acids
Peptidoglycan fragments
Mannose-rich sugars
Flagellin
LPS
Porins
Lipoteichoic acids
Mannose-rich glycans
Mycolic acid
Lipoarabinomannan
List of fungal PAMPS
Saccharides
Chitin/ Chitosan
ß-Glucan
proteins
Cell wall-related enzymes
NEP1-like proteins
Harpin proteins
Glycoprotein elicitors
GPI-anchored proteins
Secreted proteins of unknown function
Avirulence (AVR) proteins
DAMPs: Damage associated molecular patterns
Another class of molecules are associated with damage inflicted by pathogens
These DAMPs are released from the damaged tissue of the host plant and can trigger an immune response in other leaves and surrounding undamaged tissues
DAMPs are extracellular signals, termed as damage-associated molecular patterns (DAMPs) that activate the host immune response. They include cell wall or extracellular protein fragments, peptides, nucleotides, and amino acids.
SYSTEMIN is produced by wound-induced processing of a 200 aa prohormone prosystemin, which is located in the cytoplasm of vascular phloem parenchyma cells.
Plant elicitor peptides (Peps) are derived from a 92 aa precursor
Fragments of a linear polymer of 1, 4-linked α-D galacturonic acid polymer, called oligogalacturonides (OGs).
eATP acts as a signaling molecule, central role as the universal energy currency
HMG-box domain-containing proteins, AtHMGBs released from extracellular space (apoplast) after cellular damage
types of DAMPs:
· Systemin
. Plant elicitor peptides (Peps)
. Oligogalacturonides (OGs)
. Extracellular ATP (eATP)
. AtHMGB3
Effector suppressers of the plant immune system
More potent and highly selective immune suppressors
Introduced in different ways by different types of pathogens
Some are recognised by R-genes aka resistance genes for immune response in host
Bacterial secretion systems
Secretion systems are essential pathogenicity tools for bacteria because they make possible the translocation of bacterial proteins and other molecules into host plant cells.
How are effector proteins detected?
Example in A. thaliana
AvrRPM1 effector recognized by resistance gene RPM1 to mount a defense response:
In A. thaliana detected by R-genes, guard proteins (P) bind to the R gene causing a confirmation change triggering effector triggered immunity (immune response)
ZAR1 forms resistosome to induce HR response:
Zanthamona delivered
Confirmational change occurs on delivery
Changes confirmation of R gene
Forming a pentameric structure -> creates a pore causing calcium influx resulting in an immune respose
See: Adachi et al 2019
CC-NLR ZAR1 binds PBL2UMP uridylated by the Xanthomonas campestris effector AvrAC through RKS1 and undergoes conformational change, which results in ADP release from ZAR1 from the nucleotide-binding domain. This is proposed to shift NLR ZAR1 from an inactive to an intermediate state. dATP/ATP binding to intermediate ZAR1 complex results in pentamerization of ZAR1 into the resistosome wheel in which N-terminal α helices (α1, highlighted in red) become exposed to form a five-helix funnel-shaped structure (‘death switch’). The ZAR1 resistosome translocates from the cytosol into the plasma membrane (PM) and the funnel is proposed to cause HR death of the plant cell by forming toxin-like membrane pores.
Q & A
How do plants distinguish between beneficial and pathogenic organisms?
Plants can recognise beneficial/patho depending on PAMPs present
^ e.g. In funghi specific chitins cause immune response. Whereas beneficial mycorrhizae have a different chitin structure
Environmental stress can impact plant immune response and make them more susceptible to disease
Plant immune memory e.g. through vaccination but also through trans-generational resistance – plants may be able to deliver greater tolerance to their seeds?
Plants do not have specialised immune cells
Can a single pathogen attack multiple plant species?
