Botrytis cenerea the cause of grey mould disease

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Botrytis cinerea

• The cause of grey mould disease

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Botrytis cinerea

1. Introduction
2. Host range and symptoms
3. Life cycle
4. Pathogenicity
5. Host defence systems
6. Disease management

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Botrytis cinerea
Airborne Plant pathogen (reproduce by releasing
spores into the air)
Necrotrophic lifestyle  (promote the destruction
of host cells to feed on their contents)
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Botrytis cinerea

• Causes massive losses in field and
  greenhouse-grown crops !!!!
• Can grow over long periods at just above
  freezing temperatures !!!

Serious losses in more than 200 crop
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Botrytis cinerea
Destructive on mature or senescent tissues of
host
When the environment is conducive and the host
physiology changes
Vegetables (cabbage, lettuce, brocolli,
beans) Small Fruit crops ( kiwi, strawberries,
red rasberry) Oil crops (Sunflower)
Includes flowers, fruits, leaves, shoots and
even soil storage organs (carrot, sweet potato)
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Botrytis cinerea
Typical symptoms on leaves and soft fruits
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Symptoms of infection by Botrytis cinerea
Grey mould of strawberry and raspberry Fruit
Mummified 1-year-old blackcurrent fruits attached
to stem, releasing conidia amongst newly opened
flowers
Lesions arising at nodes following infection of
raspberry leaves in autumn
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Botrytis cinerea
Rapid decline in humidity with rise in temprature
causes twisting and drying of conidophores to
eject conidia
Formation stimulated by specific wavelenght of
light
To produce
Transported by air, by insect vectores or by
water droplets
In early spring
Intiation, production and dissemination are
regulated by fluctuations in temperature and
humidity
Protected by melanized rid and by ß-glucans from
dessication, UV radiation and microbial attack
High RH (relative humidity) are needed for
conidial germination and infection.
Survives within infected dead host tissues and
inside some seeds
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Botrytis cinerea - Phatogenicity
conidium
Failure at any step of signal sensing,
transduction or cellular response leads to
abnormal growth and differentiation
Germ tube
Appressorium
Quiescent Conidium spores on berry

• Production of hydrogen peroxyde
• Production of nitric acid
• Formation of proteolytic autophagosom-like
  vesicules
• Accumulation of free radicals
• massive perturbation of the redox status
• Expression of HR-specific gene Hsr203
• Activation of metacaspase

Leads to desorganized death (necrosis)

• By producing
• Phytotoxique metabolites Botrydial and
  Botcinolides
• Phytotoxique proteins NEP1-like proteins,
  Snodprot homologue, Bcspl1, Oxalic acid and
  oxalate

• Penetration by production of cell-wall-degrading
  enzymes
• Cutinase Lipase
• BcSOD1 (Superoxyde dismutase)
• NADPH-oxidases (ROS-generating systems)
• BcPG2 (endopolygalacturonase)
• PMEs (pectin methylesterase)
• Cellulase
• ß- 1,4-xylanase

Induce programmed cell death (apoptosis)
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Botrytis cinereas host defence systems
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Botrytis cinereas disease management
Many class of fungicide failed due to the genetic
plasticity and variaty of modes of attack of B.
cinerea
BCAs have restricted ranges of temperature or
humidity for maximal microbial action and they
are influenced by fluctuations responding to
changes in plant exudates and the environment
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Botrytis cinereas disease management
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Botrytis cinereas disease management
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questions ???