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Molecular Plant Immunity | 2

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Detailed, no nonsense lecture notes on molecular plant immunity, which discusses the theory of gene for gene interactions in plant pathology and critically discusses the zig-zag model of plant immunity in depth, including personalised notes with evidence from reading research papers.

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  • September 6, 2024
  • 26
  • 2023/2024
  • Class notes
  • Dr george littlejohn
  • All classes
  • Unknown
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Lecture 2 – Molecular plant immunity
Objectives:
• Discuss the theory of gene for gene interactions in plant pathology
• Critically discuss the zig-zag model of plant immunity

A food security problem… The population will reach 8.3 billion by 2030:
• 50% more food
• 30% more fresh water
• 50% more energy
• Less agricultural land
• Urbanization
• Competing land use – e.g. biofuels
• Climate Change
Highly adapted plant pathogens are particularly damaging. They have very rapid
generations in a single growing season and can out-evolve (out-compete) plant
varieties in the field. However, most plants are not susceptible to plant
pathogens because plants have very sophisticated immune systems (innate)
which combine local responses and systematic signalling.
2. Gene-for-gene hypothesis




The "gene-for-gene" hypothesis is a fundamental concept in plant pathology
that describes the molecular interactions between plants and pathogens,
particularly in the context of disease resistance. According to this hypothesis,
both the host plant and the pathogen possess specific genes that determine their
ability to interact with each other.
In more detail, when a plant is attacked by a pathogen, it recognizes specific
molecules or proteins produced by the pathogen, known as avirulence (Avr)
factors. Conversely, the plant itself carries resistance (R) genes, which code for

,proteins capable of detecting these avirulence factors. When a resistance protein
encounters its corresponding avirulence factor from the pathogen, it triggers a
defense response in the plant. This response can involve various mechanisms,
such as the activation of defense-related genes, production of toxic compounds,
or reinforcement of cell walls to prevent pathogen invasion.
The key aspect of the gene-for-gene hypothesis is the specificity of the
interaction: each resistance gene in the plant recognizes a specific avirulence
factor in the pathogen, leading to a coordinated defense response. This
specificity is thought to have evolved as a result of the ongoing co-evolutionary
arms race between plants and pathogens, where both organisms continuously
adapt and counter-adapt to each other's strategies for survival.
Overall, the gene-for-gene hypothesis provides a framework for understanding
the molecular basis of plant-pathogen interactions and has significant
implications for breeding strategies aimed at developing disease-resistant crop
varieties. By identifying and incorporating specific R genes into crop plants,
breeders can enhance their resistance to prevalent pathogens, thereby reducing
crop losses and improving agricultural productivity.




Direct recognition elicits a response. Elicitor needs to be complementary in
shape to the receptor in order to trigger a signalling cascade  hypersensitive
response. If not, cannot trigger response = susceptible to disease. Therefore, the
gene-for-gene hypothesis has a molecular basis.
3. A second wave of attack
use of a haustorium to transport effectors
nematodes with a stylet are the ones which tend to be pathogenic.

, But plants have evolved!
ZIG-ZAG MODEL OF IMMUNITY




Targets chosen based on evolution eg something crucial in the plant’s response.

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