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MBY365 Theme 4 summary
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Full summary of theme 4 (mutualist and pathogenic interactions) made using lecture notes and class notes.
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PLANT AND MICROBE INTERACTIONSINFECTION PROCESS
- Entrance through
- Stomata
- Wounds
- Enzymatic disruption - cellulases, cutinases and pectinases
- Appressoria (fungi)
- Present in apoplast
- Microorganisms do not have to enter the live cells
- Could also grow into the apoplast - space between the junction of two
pavement cells
- This could delay recognition by the plant’s immunity system
OBLIGATE ENDO-PARASITIC PLANT PATHOGENS
- Oomycetes - Pythium and Phytophothora
- Plasmodiophorids - Phytomyxea (brassicas)
- Fungi - rusts and downy mildew
EXTRACELLULAR PLANT PATHOGENS
- Plant pathogens can be classified as biotrophs, hemi-biotrophs and
necrotrophs
- Necrotrophs
- Kill the living tissue and feed off of damaged and dead tissue
- Results in expanding necrotrophic spots
- Have a broad host range
, - Virulence factors
- Plant cell wall-degrading enzymes
- Cutinases
- Host-selective toxins
- Enzymes to detoxify phytoalexins
- Common use of T2SS
- Role of quorum sensing
- Results in tissue maceration, cell killing (host specific) and degradation
of plant cuticle
- Host response is activated by oligogalacturonate products (DAMPS)
- Biotrophs
- Feed on living cells and do not kill them
- E.g. the rust fungi Basidiomycota and the powdery mildew fungi
Ascomycota
- Hemi-biotrophs feed on living tissue but in the latter stage of their life
cycle kill the host tissues - behave as both biotrophs and necrotrophs
- Pseudomonas syringae is a hemi-biotroph
- Often have a high degree of host specificity
- Virulence factors
- Cytoplasmic effectors (avirulence proteins)
- Linked to secretion systems (T3SS) and global regulators
- Have a high level of redundancy
- Plant defence system uses two branches of defence
- First one uses trans-membrane pattern recognition receptors (PRRs)
activated by PAMPs or MAMPs
- Second one uses the protein products encoded by most R genes
- Zig-zag model
- First phase - PAMPs sensed by plant PRRs causing PAMP-triggered
immunity (PTI)
- Helps in further invasion of the pathogen
- Second phase - pathogens that succeeded to overcome the plant basal
defence release their effector molecules that supports pathogen
virulence
- Effector molecules can impede PTI resulting in effector-triggered
susceptibility (ETS)
- Third phase - pathogen effector molecules are recognised by one of
the plant NB-LRR proteins leading to effector-triggered immunity (ETI)
- Fourth phase - selection helps pathogens avoid ETI either by
modification in recognised effector gene or by shedding the surface
coating of lipid and/or protein - makes plants unable to recognise them
- Natural selection can add new specificities to R genes to trigger
accelerated ETI again
, PAMP-TRIGGERED IMMUNITY
- Is the basal defence system that activates after virulent pathogen infection on
susceptible hosts
- PAMPs or MAMPs - pathogen/microbial associated molecular patterns
- Flagellin
- LPS and peptidoglycan (bacteria)
- Chitin (fungi)
- Elongation factor Tu
- Cold shock protein
- Recognition by pattern recognition receptors (PRRs) - large gene family
- Transmembrane receptor kinases
- Transmembrane receptor-like proteins
- Response
- Localised cell death
- Induced systemic resistance (ISR) - ethylene and jasmonic acid
- Localised cell wall thickening
- Release of reactive oxygen
- Successful pathogen has effectors to overcome PTI
JASMONIC ACID
- Transmits signals both locally and systemically
- Triggers
- Necrotrophic pathogens
- Wounding or insect attack
- Response
- Signal molecules (ROS; RNS)
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