L18 - Botrytis and pests Flashcards
Postharvest fungi. General characteristics
- Poor pathogens on vegetative tissue
- They need access to host tissue (wound, crack) and require that
the host has a low level of defense
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Botrytis. Can it infect any tissue? Postharvest infection?
- Yes, any tissue
- One of the few fungi that can do so
Quiescence: Is there a
Up to this phase, the plant is still in control. Nothing happens
Host plant and botrytis infection
Host cell killing is important for
Botrytis infection:
• Infection is accompanied with physiological processes that are indicative of programmed cell death (PCD)
• Chemicals or mutations (Arabidopsis) that modulate PCD influence susceptibility in quantitative manner
• Blocking or delaying PCD enhances resistance
• Promoting PCD enhances susceptibility
How does Botrytis induce host cell death?
- Phytotoxic metabolites ( botrydial , botcinic acid)
- Phytotoxic proteins (at least 10 different identified). Infiltration of phytotoxic proteins triggers programmed cell death.
BcNEP1 is very active, compared to BcNEP2 - Oxalic acid (strong acid and chelator of Ca 2+ ions)
Plant cell wall. Architecture, role of components
Plant cell walls consist of pectin, cellulose and hemicellulose (all carbohydrates)
- Cellulose provides strength
- Hemicellulose connects celluloses and is the glue between cellulose and pectin
- Pectin provides flexibility
How does botrytis decompose plant cell walls?
For each of the cell wall components, fungi possess a large and efficient enzymatic machinery that breaks down the
polymeric carbohydrates into single sugars
Pectin degrading enzymes (‘pectinases’)
Pectin degradation destroys the plant tissue AND releases sugars that fungi can use as nutrients
Which are more susceptible? Ripe or unripe fruits? What about flowers?
For each of these cell wall components, fungi possess a large and efficient enzymatic machinery that breaks down the polymeric carbohydrates into single sugars
Types of pectinases
- Pectin methyl esterase (+H2O)
- Polygalacturonase (PG) (+H2O)
- Pectin lyase (PL) (-H2O)
- PG,PL : endohydrolases -> break down the chain is small pieces
- pectin methyl esterase : exohydrolases -> provides the food for the funghis and causes the damage
What defenses does the plant have against botrytis?
- Lignin formation to fortify cell walls
- Antimicrobial metabolites that kill bacteria and/or fungi
- Plant enzymes that degrade bacterial and/or fungal cell walls
How does bortytis cope with plant defenses?
- Degrading the cell wall fortification
- Hydrolysing the antimicrobial metabolites
- Protecting its cell wall from degradation by plant enzymes
Why Botrytis is a post harvest problem? (1/2)
- The fungus can grow at low temperature (≥0.5 C)
- Fungal enzymes are active at low temperature (enzymes
promoting rot: pectinases, proteases) - Plant resistance mechanisms fail at low temperature
- When the fungus attacks an immature fruit, it induces in the
fruit the premature expression of plant genes that are normally
expressed during ripening; ripe fruit are more susceptible than
unripe fruit (!), creating a positive feedback loop for Botrytis
Why Botrytis is a post harvest problem? (2/2)
- There is no evolutionary selection pressure to be resistant
to post harvest pathogens - Once a flower is pollinated, there is little biological benefit
for the flower to remain alive/intact - Once a fruit is ripe there is no reason to remain resistant
- From the evolutionary perspective of a plant, it may be beneficial for a fruit to rot: it promotes seed dispersal!
- As long as seeds are protected from infection, post harvest pathogens are in fact beneficial for the plant
Why immature fruits are less susceptible?
- Immature fruit contain high levels of antifungal metabolites and enzymes that hydrolyze the fungal cell walls
- Immature fruit also contain high level of endopoly galacturonase inhibiting proteins (PGIPs)
- Immature fruit pectin is difficult to digest (methylation, acetylation, cross linking)
- During ripening several defense mechanisms go down:
o Breakdown of antifungal metabolites and enzymes
o Reduction of PGIP levels
o Fruit cell walls are softened by activity of expansin and degraded by activity of plant pectinases
PL ang PG
Deleting PL affects fruit firmness more than deleting PG
Deleting PL increases resistance to Botrytis susceptibility , deleting PG does not
