Lecture 7a: Plant immunity part 1 Flashcards
Why study plant immunity
- 80% of total calories consumed by human population come from only six crops: wheat, rice, maize, potatoes, sweet potatoes, and manioc (Raven, P.H. et al, 1999).
- We lose 12% of total crop yields to pathogen infection– equivalent to nine hundred million tons worldwide annually (Krimsky S. and Wrubel R., 1996)
see link:
https://www.youtube.com/watch?v=mzTE3StOHlQ
Potato blight
Blighted potato leaves caused by the oomycete
Phytophthora infestans Infection will spread rapidly through the entire plant
1.5 million people were killed by starvation during the Irish Potato Famine, 1845-52
We will now focus on another disease with a prominent place in history. The Irish Potato Famine of 1845/6 killed an estimated 1.5 million people, and forced another 2 million to emigrate. The cause was the Late Blight pathogen, Phytophthora infestans. Its name in Greek literally means Plant Destroyer! (Phyto – plant; -phthora – destroyer).The disease infects leaves, stems and tubers and it destroyed the potato harvest in Ireland in 1845. A memorial to those affected depicting frail and starving people is located on the quayside in Dublin from where many fled to new lives in America and Canada.
Against a back-drop of the figures for the Irish population between 1600 and 2000 are some more details about the famine. It is an example of a disease that was brought into a new country from its country of origin and flourished. As international trade routes developed cases like this became more common. The population of Ireland is yet to recover to pre-1845 levels, even 150 years after the outbreak (a BSPP information sheet specifically about this disease is available from www.bspp.org.uk/outreach ).
Phytophthora infestans was introduced to Ireland from South America (where the potato originates.) Cool, wet summers provided ideal conditions for the fungus to flourish
Irish labourers ate ~5.4 kg potatoes a day spread across 3 meals
Many emigrated to the United States to flee from the famine
Population yet to recover
Differences between animal and plant immune systems
Plants have no RAG (recombinant activating gene)-dependent immune system
^ no antibody system
No circulating immune cells – local recognition and response infection
– Cellular communication via plasmodesmata
– sometimes co-opted by bacteria and viruses to move systemically
Plants can pass diseases they catch to offspring – like if chicken pox was heritable
Whole plant response – Systemic acquired resistance
Plants must differentiate between pathogens and beneficial symbionts (Rhizobium and mycorrhizal fungi)
–important in nutrient poor soil and/or as biocontrol against pathogens
–Triggers of SAR?
Plant diseases: General concepts:
Signs
Symptoms
Pathogenicity
Virulence
Signs vs. symptoms
symptoms:
Visible effects of disease on plants are called symptoms. Any detectable changes in color, shape, and/or functions of the plant in response to a pathogen or disease-causing agent is a symptom.
Signs:
of plant disease are physical evidence of the pathogen, for example, fungal fruiting bodies, bacterial ooze, or nematode cysts. Signs also can help with plant disease identification.
e.g. Guinea worm – symptom is foot swelling/ sign is worm
ganoderma butt-rot symptom/ sign is the mushroom fruiting body of the fungus that caused it
Types of plant symptom
Types of symptoms:
spot – small, distinct lesion on leaf, fruit . .
(^ could be fungus/bacteria or virus non-specific sign)
blight – spots that have coalesced or merged together; more tissue being affected
rot – tissue is breaking down (fruit, roots); usually mushy, but can be dry
wilt – plant droops due to water stress; can be systemic (xylem) or due to root rot
canker – sunken lesions; usually on stems or woody tissue; but can occur on fruit
gall – masses of undifferentiated growth; usually on stems or woody tissue (branches) but can be on roots
patches, decline – terms often used in association with grasses (turf, grain crops)
Ari Sadanandom on Organic farming
Organic farming is not good for your health as it doesn’t use fungicides so it is not sustainable
^ they rely on the airbourne fungicide spread from nearby regular agricultural practicing areas
Consuming organic foods is risking the consumption of pathogens.
Mycotoxins produced by them are bad for our health though
It’s not just the disease
*As well as crop yield losses, some fungal infections are accompanied by toxin production, secondary metabolites produced by the fungus during its normal growth or when put under stress (mycotoxins)
*These mycotoxins, if consumed, can be deadly to both humans and livestock.
*If not deadly, they often give dramatic symptoms
How do pathogens enter plants?
Viruses, Viroids & Fastidious Bacteria most require vectors; a few mechanical entry
Bacteria – most enter through natural openings or wounds
Fungi & Oomycetes – enter through natural openings, wounds; by mechanical pressure or enzymes they produce; a few by vectors
Nematodes – stylets used to gain entry
Plant pathogen examples
Rice Blast: Magnaporthe grisea:
DARPA USA military want to weaponise Magnaporthe to control food production in Asia
Cladosporium fulvum — Tomato: susceptible interaction - damages leaves and prevents photosynthesis
Plant pathogen lifestyles
Heterotroph: obtain carbon and energy from other organisms
Biotroph: obtain nutrients from living host
Saprotroph (saprophyte, saprobe): obtain nutrients from dead host
Nectrotroph: infect a living host, then kill host cells to obtain nutrients
Obligate: can only grow in association with its host plant (can’t grow on artificial media)
Hemibiotroph - biotroph that switches to Nectroph
Brief history of plant disease
1863
Anton de Bary shows potato blight caused by Phytophthora
T.J. Burrill (1878)
demonstrated that fire blight of pear and
apple was caused by a bacterium, Erwinia
amylovora
Germ Theory Louis
Pasteur (1881)
TMV shown to be caused by a virus
(1898)
By the end of the 19th century, pathologists
knew why plants got sick
Disease development: Environmental conditions influence each step in the process:
for disease to occur three aspects are needed:
- susceptible host
- favourable environment
- pathogen presence
The disease triangle
Pathogen + host + environment
This is referred to as the disease triangle
-pathogen must be able to overcome plant defences
-host plant must be susceptible to pathogen
- environment must tip the balance in the favour of the pathogen
Host factors
Host factors:
*All plants can be considered hosts
*Degree of genetic uniformity – crop plants – inbred lines
*Age – affects disease development depending on plant-pathogen interaction
There are different levels of susceptibility, which include:
–Immune - cannot be infected.
–Susceptible - can be infected.
–Resistant - may or may not be infected, and the plant able to prevent the pathogen from killing it. ie. via defense compounds
Human strategies to prevent and manage plant disease
-avoid or eliminate pathogen
-make the plant resistant through genetic engineering or other methods
-manipulate the environment to favour the plant
Application of agrochemicals
The chemicals employed for crop protection may be divided into several groups according to their mode of action.
Protectant fungicides protect the plant against propagules alighting on the surface, but are ineffective against established infections; they do not normally enter the plant to any extent. Such fungicides, to be effective, must be applied before the pathogen propagules enter the host.
Systemic fungicides act quite differently: they enter the plant, become generally distributed within it, and render the tissues resistant to attack.
Eradicant fungicides enter the plant to a greater or lesser extent, killing established infections.
Genetic dissection of disease resistance pathway
see diagram in notes
^ flagella is detected as this is a key feature of bacteria triggering PTI
^ this is PAMP triggered immunity
^ to suppress PTI the pathogen makes metabolite proteins ‘virulence factors’ these are detected
( only if the plant has the relevant R gene)
R initiates Effector Triggered Immunity to stop the pathogen
PAMP (Pathogen Associated Molecular Pattern)
PAMPs are the molecules of pathogens, conserved across larger group of pathogens
Highly indispensable to the pathogens, required for their survival.
These molecules do not exist in the host.
Ex. Flagellin, EF-Tu, lipid, chitin, protein molecules of pathogens
PAMPs are elicitors of defence responses
Any substance that has the capability of activating defense responses in plants
Include components of the cell surface as well as excreted metabolites
Elicitors:
General
a) Oligosaccharide elicitors
b) Protein/peptide elicitors
Race specific
Avirulence (avr) gene
products
PRRs (Pattern recognition receptors): Perception of elicitor signals
Plasma membrane-localized recognize the presence of PAMPS in extracellular environment. Eg. FLS2, ERF, CEBiP, etc
Plant defence against pathogens
Plants respond to infection using a two-branched innate immune system
-Recognition and response to molecules common to many classes of microbes called basal disease resistance or PAMP triggered Immunity (PTI)
-Response to pathogen virulence factors
- Effector triggered Immunity (ETI)
(Liu et al.,2008)
Defining effectors
(any regulatory molecules secreted by pathogens)
Effector are any regulatory molecules secreted by pathogens
-Modifies host protein to establish their growth- Effector triggered Suppression (ETS)
Effectors perform three main functions:
- Structural role: Fungi, secrete extra haustorial molecule.
- Nutrient leakage: Eg. P. syringae HopM effector protein disrupt endomembrane trafficking
- Pathogenicity: Eg. HopA1 dephosphorylates MAP kinase results in inhibition of PTI
(Xin et al. Nature Reviews, 2018)
Effector triggered immunity:
-Against virulence effector proteins produced by pathogens
-Mediated by resistance (R) proteins
- Defence response elicited by effector recognition
- The effector molecules are recognized by R protein
Four major classes of R genes:
- NB-LRR (nucleotide binding leucine rich
repeat) genes – most important kind - Ser/Thr kinases
- Receptor-like kinases (RLKs)
- Receptor-like proteins (RLPs)
They detect effectors that are suppressing immunity
See Chisholm et al 2006
Non-Host resistance
Two mechanisms:
In case of a potentially new host, pathogen’s effectors could be ineffective, resulting in little or no supression of PTI, and failure of pathogen growth
One or more of the effector complement of the would-be pathogen could be recognized by the NB-LRR proteins of plants other than it’s coadapted host , resulting in ETI
see diagram in notes: Arabidopsis resistance to non-adapted powdery mildew Blumeria graminis f. sp. Hordei
(Jones et al., 2006)
