Fungi-plant Interactions Flashcards
The factors that influence disease susceptibility
Severity of environment
Pathogen: virulence, abundance
Host susceptibility
If any of these are 0, disease wont develop
Method of fungal arrival and entry into plant
Spores
Types of spores
Thin walled
Resting spores
Sclerotia
Zoospores
Different methods of spore travel
Wind
Rain splash
Animal vectors
May need certain stimulants or conditions to then germinate
Describe use of mycelium when spreading fungi
Some fungi can arrive as spores
Colonise wood
Then spread between other hosts via a root graft
Describe infection courts
Wounds
Natural openings e.g. stomata (common with obligate parasites)
Intact surfaces (common with pathogens and facultative parasites)
Methods of plant tissue penetration
Appressorium
Vectors
Natural openings
Describe fungal appressorium for penetrating plant tissue
- hyphae grows along plant cuticle out of spore
- produces appressorium and penetration peg = mechanical pressure (and may release enzymes)
- haustoria grows within cell to extract plant nutrients (central body with extending lobes)
Describe vectors penetrating plant tissue
Can occur via animal vectors feeding/oviposition
- create infectious courts fungus can enter through
E.g. bark beetles, twig crotches that open the xylem and o.ulmi = Dutch elm disease
Describe natural openings and plant tissue penetration
- spore on leaf surface releases hyphae
- hyphae dont grow with leaf grooves but across them = figmatropic response
- increases chance of finding stoma
What are the two categories of host resistance
Preformed defence
Induced defence
Forms of plant preformed defence
Thick cell walls
Cutin = Suberin or waxes covering plant exterior
Bark = physical and chemical defence
Phytoanticipins = inhibitory compounds against pathogens
What are the 2 forms of induced defence
Rapid
Slower
Forms of rapid induced defence
- oxidative outburst
- nitrous oxide production
- cross linking of cell wall proteins
- production of callose
- hypersensitive response
Affect of nitrous oxide production on plant defence
Signalling molecule
Initiate programmed cell death of infected cells
Affect of production of callose of plant defence
A polysaccharide that sits between plasma membrane and cell wall to prevent fungal entry
What is the hypersensitive response for plant defence
Increased production of antagonistic chemicals
Will also cause plant cells to die
Defence mostly against biotrophic pathogens as they depend on living cells
Forms of slow induced defence in plants
- phytoalexins
- lignification
- suberization
- hydroxyproline-rich glycoproteins (HGRPs)
- pathogenesis related proteins (PRPs)
- system resistance
Describe role of phytoalexins in slow plant induced defence
Provide future resistance to pathogen that has previously infected plant
Describe role of suberization in slow induced plant defence
Turning cell walls into cork metrical by producing Suberin
What is innoculum potential?
Whether disease develops
- increasing the number of spores increases the chance it will reach a plant and that the plant wont be able to defend itself
- varies between disease and multiple factors can affect
What is a necrotroph
Lives inside dead plant cells
What is a biotrophs
Found within living cells
Relies on a balanced relationship
Methods of necrotroph establishment and exploitation
Enzymes: damping off
Toxins
Vascular wilts
Provides fungus with nutrients
Cell death can be extensive or localised
What is enzymatic damping off
Often with oomycetes
Pectin is broke down (middle lamellae) = cells become soft water tissue and fruit has soft rot
Role of toxins in necrotrophic establishment and exploitation.
Cause tiny lesions on the leaves that spread
Often slow but can have fast action
Tissue remains dry but discoloured
Describe the role of vascular wilting on necrotrophic establishment and exploitation
- Vascular wilt caused by damage to vascular tissue
- Produce toxins in xylem..spreads to leaves = loss of transport control
- results in death
E.g. of necrotrophic fungus
Dutch elm disease = wilt disease
- Ophiostoma ulmi 1910-1940
- killed 10-40% - O.novo-ulmi replaced O.ulmi in 1940s
- more aggressive = most elms in Britain dead
Spread via elm bark beetles
= xylem blocked by gums, tyloses and fungal material
Whats tyloses?
Outgrowths of parenchyma cells in xylem
Occurs when stressed
How biotrophs cause establishment and exploitation in plant tissue
Abstract nutrients by ‘switching on’ enzymes
Later functioning of host
E..g of biotroph altering plant functioning
Green islands = increase of chlorophyll
Longer photosynthesis than there should be to feed the fungus
E.g. of biotrophic parasites
Rusts
Smuts
Downy mildew
Powdery mildew
Hemibiotroph
Pathogenic fungi with biotrophic life phase whilst it establishes itself in host
E.g. of hemibiotroph
Rice blast, magnaporthe oryzae
- spore produces appressorium and peg
- haustoria produced: causes lesions
- spreads via pants plasmodesmata
Initially feeds on living cells then causes death
- week to germinate
- 20,000 spores within one leaf lesion
Polycyclic disease
Multiple infection cycles per year
Exit/survival strategy of necrotroph
Free from competition initially = slow growing in passive occupation
Combat fungi arrive = colonisation rate decreases
- if fungus has enough territory and resistant spores will win
Saprotrophic = grow out into soil and are combative
OR
Avoid combat and extend though soil as mycelial cord or rhizomorph
Difference in life strategies in necrotrophic and biotrophic
Biotroph more K selected than necrotroph
Parasites stress tolerant
Emerging infectious diseases emergence
Pathogenic fungi often little threat in local region where they co-evolve with hosts
Emerge when:
- increase in incidence, host range or geographical range
- altered pathogenesis
- newly evolved
- newly discovered
E.g. if emerging infectious disease
Potato blight
From South America to Europe
1million people dead
1 million emigrated
