Plant Immunity Flashcards
What are 4 forms of biotic stress that plants undergo?
Herbivores, fungi, viruses, and bacteria.
From where do pathogens infiltrate plants?
The stomata on the leaves of the plant.
Why is it easier for pathogens to infiltrate plants?
Plants are sessile.
When is a plant protected against a pathogen.
If an avirulent (Avr) allele in a pathogen responds to an R allele in the host plant, the host plant will have resistence, making the pathogen avirulent.
Which two different types of microbial signals can plants recognise, how are they recognised, and to what response do they lead?
PAMPs/MAMPs can be recognised by PRRs and leads to PAMP-triggered immunity (PTI). Effector proteins can be recognised by resistance (R) proteins and leads to effector-triggered immunity (ETI). All micro-organisms show PAMPs/MAMPs and lead to PTI. However, only specialised pathogens can use effector proteins, which leads to ETI.
What is the effect of ETI?
ETI has a macroscopic effect, namely a hypersensitive response (HR), which equals to cell death.
Name some examples of PAMPs/MAMPs.
Flagellin in bacterial flagella, peptidoglycan in bacterial cell walls, EF-Tu (bacterial elongation factor for protein translation), chitin in fungal cells walls, and oligosaccharides in fungal and plant cell walls.
What is the signalling cascade of flagglin recognition in plant immunity.
The PAMP flagellin can be recognised by the FLS2 PRR, after which it dimerises with BAK1, which is a co-receptor of several PRRs. Subsequently, BIK1, a receptor-like cytoplasmic kinase (RLCK) is recruited and mitogen-activated protein kinases (MAPKs) and calcium-dependent protein kinases (CDPKs) are activated.
How do specalised pathogens, like certain bacteria or fungi, affect PTI in plants?
With specialised pathogens, like certain bacteria or fungi, the fungi grows inside the plant cell and secretes effector proteins, or the bacterium secretes effector proteins inside the plant cell using a pilus. These effector proteins inhibit the PTI response and can be recognised by an R-proteins’ nucleotide-binding leucine-rich repeats (NB-LRR), resulting in an ETI response. These effector proteins have an effect on a lot of different parts of the PTI. For example, the effector proteins can inhibit PRRs and BAK1, MAPK, and GRP7, which are important in mRNA translation.
How do R proteins interact with effectors? And how does a plant “fool” a pathogen with this?
R proteins can interact with effectors in two ways, namely a direct interaction (ligand-receptor model) and an indirect interaction (guard model). With indirect interaction, effectors modify a plant protein, the “guardee”, to increase their virulence. However, plants have evolved to produce decoys. These decoys are effector-targeted plant proteins without a direct role in defence, solely evovled for pathogen recognition. Thus, the pathogen is fooled.
How do resistance (R) genes function in resistant plants?
Resistant plants have resistance (R) genes, encoding R proteins that monitor a change in the target proteins and initiate a hypersensitive response leading to inhibition of growth of that pathogen.
What is the standard signalling cascade in plant immunity?
The plant immune response begins with a pathogen (insect herbivory, necrotrophic microorganisms, or biotrophic microorganisms), which gets recognised by a receptor. Subsequently, biosynthesis of a certain blend of plant defence hormones (jasmonic acid (JA), ethylene, or salicylic acid (SA)) occurs. Then, these defence hormones are recogised by specific receptors. Subsequently, specific transcription factors are activated, a specific response gene set is transcribed, and a specific defence response occurs (respectively, genes for wound-response and anti-insect proteins, ethylene-responsive gene expression, and pathogen-related (PR) gene expression). Jasmonic acid-mediated defence does not involve cell death, because it is a defence against necrotrophic organisms, which grow on dead plant material. Salicylic acid-mediated defence involves cell death, which only works against biotrophic microorganisms, which grown on living plant tissue.
On which responses is plant immunity based?
Plant immunity is based on a hypersensitive response (cell death), and the production of pathogen-related proteins (toxic proteins and enzymes that degrade bacterial/fungal cell walls).
Which microorganisms does salicylic acid target in plant immunity?
Salicylic acid is involved in resistance against viruses (e.g. TMV), biotrophic bacteria, and biotrophic fungi.
Plant responses can be divided into two categories. Give these two categories and explain what they entail.
Plant responses can be divided into a local defence and a systemic defence. The local defence, which happens at the site of inflammation, consists of a hypersensitive response (HR) and the secretion of antimicrobial secondary metabolites (e.g. alkaloids in some plant species, glucosinolates in Arabidopsis), antimicrobial proteins (e.g. defensins, pathogenesis-related (PR) proteins), and antimicrobial cell wall-degrading enzymes (e.g. chitinases and B-glucanases). The systemic defence consists of systemic acquired resistance (SAR; depends on salicylic acid and ethylene) and induced systemic resistance (ISR; depends on jasmonic acid and ethylene).
