HOST-MICROBE INTERACTIONS [B-B2HOMI]
~complete summary~
This summary has been based on lectures, tutorials, How to science and computer
practicals, giving an precise overview of all the information you need for your exam in a
structured way to grasp main mechanisms and compare PLANTs and ANIMALs
responses.
• p. 2-14: clear summary per theme, divided by PLANT and ANIMAL
[pathogens – innate immunity – adaptive/acquired immunity – distinguishing friend from foe – microbiome]
• P. 15-17: clear comparison of PLANT and ANIMAL immunity characteristics
• P. 18-19: additional information from tutorial
• P. 20: clear overview of all CAPs and main take home messages
• P. 21: summary of “how to science” with clear overview of experimental steps
, ~ PLANT COMPONENTS ~
~ 1A. PLANT PATHOGENS~
▪ Nematodes: multicellular animals, feeding stylet [biggest pathogen]
▪ Viruses: non-cellular, packaged nucleic-acids [smallest pathogen]
▪ Bacteria: prokaryotes
▪ Fungi & oomycetes: filamentous eukaryotes, reproduce (a)sexually by spores
Nutritional/lifestyle strategies
1. Biotroph Obtains nutrients from living host cells (haustoria & effectors for immune evasion)
2. Hemi-biotroph Beins as biotroph and later switches to necrotrophic phase
3. Necrotroph Kills host cells and feeds on released nutrients (toxins and cell-wall degrading enzymes)
Saprophyte* lives off dead organic matter ≠ pathogen!
Parasitic plants: penetrate host tissue and extract nutrients/water
Pests: insects and other animal that cause plant damage
Plant disease: impairment of plant growth, physiology or other vital functions
(BIOTIC) → caused by pathogenic micro-organisms (fungi, bacteria, viruses, nematodes)
(ABIOTIC) → caused by environmental stress (drought, flooding, heat/cold, nutrient deficiency)
• Symptoms: discoloration (chlorosis = yellowing), wilting (clogged vascular tissue), tissue death (necrosis)]
EXAMPLES
I) Powdery mildew [fungi = biotroph]
▪ Grows on leaf surface as mycelium, produces conidia for asexual spreading OR ascospores for survival under harsh conditions
▪ Uses Haustoria to extract nutrients from epidermal cells
II) Potato late blight [oomycete = hemi-biotroph]
III) Grey mold [fungi = necrotroph]
IV) Bacterial speck
▪ Enters leaves through stomata or wounds, spreads using flagella and multiplies intracellularly
V) Tumors
▪ Soil bacteria activated by chemical compounds released by wounded plant cells and attaches to plant tissue
▪ T-DNA (from plasmid) injection and integration into plant genome induces hormone production for uncontrolled proliferation
VI) Tobacco mosaic virus
▪ Uses host replication machinery and new virus particles self-assemble and spread to other cells via plasmodesmata and phloem
~ 1B. PLANT VIRULENCE FACTORS ~
> Pathogens can obtain nutrients from living cells and contain virulence/pathogenicity genes
> Plant pathogen entry: via stomata, wounds, feeding stylets, or haustoria, enabling tissue colonization and nutrient acquisition.
▪ Virulence genes= encode factors that enable infection, colonization, evade host defense or cause disease
[toxins, enzymes, effectors, adhesion proteins, motility, invasion or penetration structures]
VIRULENCE FACTORS/GENES
1. Flagellum Motility to reach infection site = trade-off as conserved epitope for immune recognition
2. Type III secretion system (T3SS) Structure to inject effectors/proteins/DNA into host cells
3. Extracellular polysaccharides Adhesion to surfaces, formation of biofilms or capsules
4. Appressorium At end of germ tube, creates high pressure for penetration peg and attachment
5. Haustorium Biotrophic feeding structure
[spore → germ tube → appressorium → penetration peg → haustorium/extracellular matrix/plant plasma membrane]
Physical surface recognition: for positioning and host specificity
Cell-wall degrading enzymes: break down cellulase, pectinase, cutinase to facilitate invasion of necrotroph
Toxins: alter membrane permeability, inhibit essential cellular processes (enzyme activity, nutrient uptake)
EXAMPLE – HORMONE MANIPULATION
> Virulence genes located on TI plasmid mediate transfer of T-DNA into plant cells
> T-DNA enters nucleus and is incorporated into host genome, where transcription causes excess hormone production
, ~ 3. INNATE IMMUNE SYSTEM ~
= race between plant (immune recognition and response activation) and pathogen (inhibition and evasion)
= often when a plant is more resistant to necrotrophy, it is more resistant to a biotroph (immune response antagonist)
• PTI= against necrotroph, polygenic resistance (partial)
• ETI= against biotroph, complete resistance (R-gene and AVR-gene)
Zig-zag model of plant-pathogen interaction:
1. Pattern triggered immunity (PTI) Pathogen recognition receptors (PRRs) recognize PAMPs as firs line of defense
2. Effector triggered susceptibility (ETS) Pathogen produced effectors suppress downstream cellular signaling
3. Effector triggered immunity (ETI) Resistance genes recognize effectors, highest defense
I. PTI – PAMP RECOGNITION & DEFENSE MECHANISMS
Polygenic resistance: controlled by multiple genes, providing broad but partial protection
> Depends on presence of specific components, thus natural variation in resistance/susceptibility
> pathogen can still multiply and cause symptoms
Pattern recognition receptors (PRRs): located on plasma membrane
> cause Ca2+ influx, kinase cascade, ROS production for defense & transcriptional response
[BIK1 activated by phosphorylation – activates NADPH oxidase, produces reactive oxygen species]
> recognize EF-Tu, flagellin, lipopolysaccharide (LPS), peptidoglycan and chitin as PAMPs
1. Leucine-rich repeat receptor kinase
- Extracellular: leucine-rich repeat domain that recognizes conserved microbial elements
- Intracellular: kinase domain for signal cascade to response activation
→ FLS2 + Flagellin | EF-Tu
2. LysM receptor proteins
- recognize N-acetylglucosamine (Glc-Nac) backbone containing molecules
→ CERK1 + peptidoglycan/chitin | LPS | NFR1 + Nod factor
Phenylpropanoid pathway: rapid PRR-triggered response activation multiple enzymes
(1) produces secondary metabolites, (2) enhance ROS production, (3) cell wall reinforcement
= physical barrier and chemical defense
DEFENSE RESPONSES
Peroxidase & lignin production Detoxifies ROS and strengthens cell wall
Callose deposition Papillae formation at infection site reinforces against penetration peg (polysaccharide)
Antimicrobial compounds - phytoanticipins, preformed
(kill or inhibit) - phytoalexins, induces by infection
Cell wall degrading enzymes Chitinase, glucanases and PG-inhibiting proteins in reaction to PG from fungi
II. ETS – EFFECTOR DEPENDENT INHIBITION
= microbial effector suppress immune signaling and/or enhance pathogen viability (directly affect host processes!)
▪ T3SS (bacteria): encoded in single operon
▪ Haustoria or hyphae tips (fungi): intimate host-pathogen membrane interface for exchange
▪ Feeding stylet (nematode): intracellular injection
1. Altering plant behaviour/development
- Reopen stomata (entry), interfere with plant hormone production (gibberellin, auxin, ethylene), induce necrosis
- Signal interference, inhibit enzyme activity or alter organel structure/function and transcription activity
→ loss of effector target increases host resistance
2. Enhanced pathogenicity
- Effector genes in dynamic genome regions (duplications, transposons, repeats and relatively few other functional genes)
→ enable rapid effector innovation and diversity
3. Lifestyles
- transition (biotrophy to necrotrophy) with different effector set via coordinated temporal gene expression
~complete summary~
This summary has been based on lectures, tutorials, How to science and computer
practicals, giving an precise overview of all the information you need for your exam in a
structured way to grasp main mechanisms and compare PLANTs and ANIMALs
responses.
• p. 2-14: clear summary per theme, divided by PLANT and ANIMAL
[pathogens – innate immunity – adaptive/acquired immunity – distinguishing friend from foe – microbiome]
• P. 15-17: clear comparison of PLANT and ANIMAL immunity characteristics
• P. 18-19: additional information from tutorial
• P. 20: clear overview of all CAPs and main take home messages
• P. 21: summary of “how to science” with clear overview of experimental steps
, ~ PLANT COMPONENTS ~
~ 1A. PLANT PATHOGENS~
▪ Nematodes: multicellular animals, feeding stylet [biggest pathogen]
▪ Viruses: non-cellular, packaged nucleic-acids [smallest pathogen]
▪ Bacteria: prokaryotes
▪ Fungi & oomycetes: filamentous eukaryotes, reproduce (a)sexually by spores
Nutritional/lifestyle strategies
1. Biotroph Obtains nutrients from living host cells (haustoria & effectors for immune evasion)
2. Hemi-biotroph Beins as biotroph and later switches to necrotrophic phase
3. Necrotroph Kills host cells and feeds on released nutrients (toxins and cell-wall degrading enzymes)
Saprophyte* lives off dead organic matter ≠ pathogen!
Parasitic plants: penetrate host tissue and extract nutrients/water
Pests: insects and other animal that cause plant damage
Plant disease: impairment of plant growth, physiology or other vital functions
(BIOTIC) → caused by pathogenic micro-organisms (fungi, bacteria, viruses, nematodes)
(ABIOTIC) → caused by environmental stress (drought, flooding, heat/cold, nutrient deficiency)
• Symptoms: discoloration (chlorosis = yellowing), wilting (clogged vascular tissue), tissue death (necrosis)]
EXAMPLES
I) Powdery mildew [fungi = biotroph]
▪ Grows on leaf surface as mycelium, produces conidia for asexual spreading OR ascospores for survival under harsh conditions
▪ Uses Haustoria to extract nutrients from epidermal cells
II) Potato late blight [oomycete = hemi-biotroph]
III) Grey mold [fungi = necrotroph]
IV) Bacterial speck
▪ Enters leaves through stomata or wounds, spreads using flagella and multiplies intracellularly
V) Tumors
▪ Soil bacteria activated by chemical compounds released by wounded plant cells and attaches to plant tissue
▪ T-DNA (from plasmid) injection and integration into plant genome induces hormone production for uncontrolled proliferation
VI) Tobacco mosaic virus
▪ Uses host replication machinery and new virus particles self-assemble and spread to other cells via plasmodesmata and phloem
~ 1B. PLANT VIRULENCE FACTORS ~
> Pathogens can obtain nutrients from living cells and contain virulence/pathogenicity genes
> Plant pathogen entry: via stomata, wounds, feeding stylets, or haustoria, enabling tissue colonization and nutrient acquisition.
▪ Virulence genes= encode factors that enable infection, colonization, evade host defense or cause disease
[toxins, enzymes, effectors, adhesion proteins, motility, invasion or penetration structures]
VIRULENCE FACTORS/GENES
1. Flagellum Motility to reach infection site = trade-off as conserved epitope for immune recognition
2. Type III secretion system (T3SS) Structure to inject effectors/proteins/DNA into host cells
3. Extracellular polysaccharides Adhesion to surfaces, formation of biofilms or capsules
4. Appressorium At end of germ tube, creates high pressure for penetration peg and attachment
5. Haustorium Biotrophic feeding structure
[spore → germ tube → appressorium → penetration peg → haustorium/extracellular matrix/plant plasma membrane]
Physical surface recognition: for positioning and host specificity
Cell-wall degrading enzymes: break down cellulase, pectinase, cutinase to facilitate invasion of necrotroph
Toxins: alter membrane permeability, inhibit essential cellular processes (enzyme activity, nutrient uptake)
EXAMPLE – HORMONE MANIPULATION
> Virulence genes located on TI plasmid mediate transfer of T-DNA into plant cells
> T-DNA enters nucleus and is incorporated into host genome, where transcription causes excess hormone production
, ~ 3. INNATE IMMUNE SYSTEM ~
= race between plant (immune recognition and response activation) and pathogen (inhibition and evasion)
= often when a plant is more resistant to necrotrophy, it is more resistant to a biotroph (immune response antagonist)
• PTI= against necrotroph, polygenic resistance (partial)
• ETI= against biotroph, complete resistance (R-gene and AVR-gene)
Zig-zag model of plant-pathogen interaction:
1. Pattern triggered immunity (PTI) Pathogen recognition receptors (PRRs) recognize PAMPs as firs line of defense
2. Effector triggered susceptibility (ETS) Pathogen produced effectors suppress downstream cellular signaling
3. Effector triggered immunity (ETI) Resistance genes recognize effectors, highest defense
I. PTI – PAMP RECOGNITION & DEFENSE MECHANISMS
Polygenic resistance: controlled by multiple genes, providing broad but partial protection
> Depends on presence of specific components, thus natural variation in resistance/susceptibility
> pathogen can still multiply and cause symptoms
Pattern recognition receptors (PRRs): located on plasma membrane
> cause Ca2+ influx, kinase cascade, ROS production for defense & transcriptional response
[BIK1 activated by phosphorylation – activates NADPH oxidase, produces reactive oxygen species]
> recognize EF-Tu, flagellin, lipopolysaccharide (LPS), peptidoglycan and chitin as PAMPs
1. Leucine-rich repeat receptor kinase
- Extracellular: leucine-rich repeat domain that recognizes conserved microbial elements
- Intracellular: kinase domain for signal cascade to response activation
→ FLS2 + Flagellin | EF-Tu
2. LysM receptor proteins
- recognize N-acetylglucosamine (Glc-Nac) backbone containing molecules
→ CERK1 + peptidoglycan/chitin | LPS | NFR1 + Nod factor
Phenylpropanoid pathway: rapid PRR-triggered response activation multiple enzymes
(1) produces secondary metabolites, (2) enhance ROS production, (3) cell wall reinforcement
= physical barrier and chemical defense
DEFENSE RESPONSES
Peroxidase & lignin production Detoxifies ROS and strengthens cell wall
Callose deposition Papillae formation at infection site reinforces against penetration peg (polysaccharide)
Antimicrobial compounds - phytoanticipins, preformed
(kill or inhibit) - phytoalexins, induces by infection
Cell wall degrading enzymes Chitinase, glucanases and PG-inhibiting proteins in reaction to PG from fungi
II. ETS – EFFECTOR DEPENDENT INHIBITION
= microbial effector suppress immune signaling and/or enhance pathogen viability (directly affect host processes!)
▪ T3SS (bacteria): encoded in single operon
▪ Haustoria or hyphae tips (fungi): intimate host-pathogen membrane interface for exchange
▪ Feeding stylet (nematode): intracellular injection
1. Altering plant behaviour/development
- Reopen stomata (entry), interfere with plant hormone production (gibberellin, auxin, ethylene), induce necrosis
- Signal interference, inhibit enzyme activity or alter organel structure/function and transcription activity
→ loss of effector target increases host resistance
2. Enhanced pathogenicity
- Effector genes in dynamic genome regions (duplications, transposons, repeats and relatively few other functional genes)
→ enable rapid effector innovation and diversity
3. Lifestyles
- transition (biotrophy to necrotrophy) with different effector set via coordinated temporal gene expression
