Lecture 21: Fungal Pathogens of Plants Flashcards

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1
Q

What are different types of plant disease?

A
  1. Fruit rot
  2. Stalk rot
  3. Mildew
  4. Wilt
  5. Leaf blight
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2
Q

Why study plant microbe interactions?

The importance of plant disease

A
  1. Agriculture
    a. Pathogens can impair crop quality
    b. Can drastically reduce crop yield
    (e. g., Irish potato famine)
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3
Q

What are the different forms of fungal infections? What is there economic impact?

A
1. Air-borne fungi: e.g., Blumeria spp. on 
   small grain cereals - causes mildew
2. Soil-borne fungi: e.g., Fusarium and 
    Verticillium - often causes wilt 
    diseases
  1. Economic impact:
    a. >50% of breeding for disease
    resistance is against fungal diseases
    b. reduced biomass and yield
    c. Cause recurrent seasonal epidemics
    (e.g., small grain cereals)
    d. soil-borne fungi tends to cause more
    chronic infections
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4
Q

What is Oomycetes?

A
  1. NOT FUNGI
  2. Dispersed via asexual zoospores
  3. Produce oospores (sexual
    reproduction)
  4. Cellulose cell walls
  5. Diploid
  6. Cause downy:
    a. mildew diseases
    b. blights
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5
Q

What are the three strategies used by fungi to infect plants?

A
  1. Biotrophic
    a. require living host to grow and
    reproduce
    b. Includes obligate parasites that only
    grow on specific host (e.g.,
    Blumeria)
  2. Necrotrophic
    a. Kill host cells through action of lytic
    enzymes and toxins
    b. colonize and reproduce on dead tissue
  3. Hemi-biotrophic
    a. grow biotrophically at first then
    switch to necrotrophy

SEE SLIDE FOR DETAILED TABLE OF

  1. attack means
  2. specific features
  3. host range
  4. examples
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6
Q

What are the 4 key stages of fungal pathogenesis?

A
  1. Attachment
  2. Penetration
  3. Invasive growth within plant
  4. Suppression/inactivation of host
    defences
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7
Q

What is the infection cycle of rice blast fungus? How long does it take?

A
  1. Invasive growth
  2. Lesions
  3. Sporulation
  4. Attachment
  5. Germination
  6. Hooking
  7. Appressorium
  8. Penetration

5-7 DAYS

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8
Q

How does a fungus penetrate the cuticle and cell wall?

A

Appressoria can generate v. high turgor pressure (6-8 Mpa) - allowing penetration

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9
Q

What is an example of biotrophic pathogens?

A

Plant: Barley
Pathogen: Blumeria graminis
Plant: Arabidopsis thaliana
Pathogen: Erysiphe cruciferarum

  1. Infects:
    a. barley
    b. wheat
    c. rye
    d. oat
  2. Several ‘forma specialis’ (taxonomic
    grouping applied to fungi that have
    adapted to specific host)
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10
Q

What are fungal haustoria’s?

A
1. Specialised structures formed   
   specifically by BIOTROPHIC and 
   HEMITROPHIC fungi
   a. e.g., graminis 
2. Increase SA of contact between     
    fungus and host cell = exchange of: 
   a. nutrients  
   b. and signal molecules
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11
Q

What is the structure of haustoria?

A
  1. invaginate the cell following penetration
  2. fungus remains extracellular
  3. two membrane systems from the
    plant and fungus
  4. separated by extracellular haustoria
    matrix
  5. Site of delivery for effector molecules
    and uptake of nutrients
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12
Q

What is an example of a biotroph that doesn’t produce haustoria

A
  1. Tomato leaf mould pathogen:
    Cladosporium fulvum
  2. Extracellular hyphae do form contacts
    with leaf mesophyll cells
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13
Q

What is an example of a necrotoph

A
  1. Grey mould fungus: Botrytis cinerea
  2. Macerates plant tissue
  3. Broad host range (~200 diff plants)
  4. Prod. cell wall degrading enzymes that
    destroy plant tissue in advance of
    colonising hyphae
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14
Q

What determines virulence?

A
1. Various effector (Avr) proteins from 
   haustorial biotrophic pathogens 
   a. Proteins DIRECTLY cross the 
       extrahaustorial membrane (1) OR enter 
       cell endomembrane system via 
       vesicles (2)

Oomycetes prod. 2 distinct classes of effector:
1. RxLRs - have RxLR motif followed by
an E/D-rich region which target the
proteins to the host cytoplasm. > 100
RxLR proteins in Phytophthora
2. “Crinklers” (CRNs). Translocated into
host nucleus and cause leaf-crinkling
and cell-death phenotype

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15
Q

How does the “Magnaporthe oryzae” effector Slp1 suppress chitin-triggered defence response in rice?

A
  1. Rice recognises chitin - a fungal PAMP
  2. Chitin oligosaccharides are bound by chitin elicitor bind protein (CEBiP) initiating defence (=PTI)
  3. Rice blast fungus Magnaporthe oryzae secreted LysM protein 1 (Slp1) binds to chitin and suppresses chitin-induced plant immunity
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16
Q

What is Avenacinase and what does it do?

A
  1. it is from Gauemannomyces. graminis
    f.sp avenae.
  2. degrades antifungal compound
    avenacin
  3. AVN1 encodes: Avenacinase (beta-
    glucosyl hydrolase
  4. AVN1 is required by G. graminis var
    avenae for infection of oats
17
Q

How can plants resist fungal disease?

A
  1. Breeding plants began with Sir Rowland Biffen - identified single recessive gene for resistance against “wheat yellow rust” caused by “Puccinia striiformis”
  2. “Green Revolution” of 20th century lead to achievements in wheat, maize, and rice traits:
    a. increase yield
    b. improve quality
    c. Multiline varieties for resistance
    d. Tolerance to abiotic stresses
18
Q

Examples of resistance genes against wheat leaf rust, alongside their “boom” and “bust”

A
  1. Lr1, 13
    a. boom = 1970
    b. bust = 1973
  2. Lr13, 17
    a. boom = 1971
    b. bust = 1975
  3. Lr17, 27+31
    a. boom = 1973
    b. bust = 1977
  4. Lr13, 26
    a. boom = 1981
    b. bust = 1984
  5. Lr23, 26
    a. boom = 1982
    b. bust = 1985
  6. Lr14b, 27+31
    a. boom = 1992
    b. bust = 1994