Lecture 4 Flashcards

1
Q

What are the plant surface composed of

A
  • cellulose as part of their epidermal cells of roots & in intercelluar spaces
  • OR cuticle covering the epidermal cell wall
  • somtimes additional layer of wax/wax crystals outside of cuticle (common in younger plants)
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2
Q

Weapons used by plant pathogens

2 types and what are they know as

A

Virulance factors

  • physical
  • chemical - enzymes
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3
Q

how do plants pathogens use physical weapons

A
  • in lecture 3
  • mechanical forces: melanin
    production by Alternaria, Cochliobolus, Colletotrichum, Magnaporthe
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4
Q

how do plants pathogens use Chemical weapons
(4 things)

A
  • Enzyme
  • microbial toxins
  • growth regulators
  • polysaccharides.
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5
Q

how do plants pathogens use enzymes as weapons

A
  • large protein molecules that catalyze organic reactions in living cells.
  • enzymes could be present in cells at all times
  • (fungi can produce enzymes that degregate cell wall substances)
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6
Q

Cutin vs Cutinase

an enzyme

A

Cutin: main component of cuticle (on a plant)

Cutinase: the enzyme produced by pathofens to degrade cutin

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7
Q

Pectin vs pectinase

an enzyme

A

Pectin: used by plants as the main componet of middle lamella. Works as cement to connect cells with eahcother

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8
Q

other examples

  • Cellulose vs cellulase
  • Hemicellulose vs hemicellulases
  • lipids vs lipase

An enzyme

A
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9
Q

Lignin

& how many types of pathogen can degrade it

A
  • at the middle lamella & seondary cell wall of xylem vessels & fibers that strengthen the plants. Could also be present in epidermal cell wall
  • makes up 15-38% (woody plants)
  • Only a small group of pathogens can degrade lignin. About 1/4th of the fungi that can degrade lignin can not make use of it. eg: white
    rot fungi/ soft rot cavities in woody plants.
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10
Q

Microbial toxins

A
  • low molecular weight compounds secreted by pathogens/microbes.
  • Fungi produces mycotoxins
  • both host-selective & nonhost-selective
  • they act directly on host protoplasts -> seriously damagin/killing plant
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11
Q

how does microbial toxins work

A
  • they act directly on host protoplasts -> seriously damagin/killing plant
  • by affecting cell membrane permeability to injoure cells.
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12
Q

examples of nonhost selective toxins

4 examples

A

tabtoxin
- bacterium Pseudomonas syringae
pv. tabaci that causes wildfire disease of tobacco

Phaseolotoxin
- P.syringae pv. phaseolicola, the cause of halo blight of bean

Tentoxin
- fungus Alternaria alternata causing spots and chlorosis on plants

Cercosporin (fungus Cercospora).

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13
Q

examples of host-selective toxins

3 examples

A

Victorin or HV toxin
- Cochliobolus/Helminthosporium victoriae infecting oats)

T toxin
- Biploaris maydis race T,
causing southern corn leaf blight

HC toxin
- Biploaris zeicola causing northern leaf spot and ear rot in corn

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14
Q

Growth regulators

A

small number of naturally occurring compounds that act as hormones and are involved in plant growth

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15
Q

how does pathogens cause hormonal imbalance to plants growth regulators

A
  • plant pathogens may produce the same growth regulators as those produced by plants (causing them to grow bigger but that means thet are weaker)
  • plant pathogens can also produce substances that stimulates or retard the production of growth regulators or inhibitors by the plant.
  • even the slightest different from normal growth factor concentrations can bring huge chnages in plant growth pattern
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16
Q

Auxins

grwoth factor

A

** indole-3-acetic acid (IAA)**
- required for cell elongation and differentiation and absorption of IAA to the cell membrane which affects the permeability of the membrane.
- produced naturally and moves rapidly from young green tissue to older tissues but constantly destroyed by the enzyme** indole-3-acetic acid oxidase**

Increased IAA level
- eg. Clubroot pathogen (Plasmodiphora brassicae) of brassicas
- crown gall bacterium (Agrobacterium tumefaciens)
- corn smut fungus (Ustilago maydis)
- cedar apple rust(Gymnosporangium juniperi-virginianae)

these pathogens don’t only increase the level of IAA in host but are also capable of producing
IAA themselves.

17
Q

Crown gall

A
  • tumors develop when crown gall bacterium enters the fresh wounds of susceptible host
  • phenolic compounds are produced around the wounded spot
  • agrobacterium dont invade the cells but attach to cell wall. In response to phenolic compounds beging processing their DNA in their Ti plasmid

READ MORE ON THIS AND THE OTHER ONES LISTED IN LECTURE

18
Q

Cytokinins

grwoth factor

A
  • necessary for cell growth and differentiation.
  • inhibit breakdown of proteins and nucleic acids, thereby causing inhibition of senescence.
  • Cytokinin activity increases in clubroot galls, crown galls, in smut and rust galls.
  • Cytokinins are also partly
    responsible for leafy gall disease.
19
Q

Leafy gall disease

A

Rhodococcus fasians
- centres of shoot overproductions and short growth inhibition
- produce auxins, cytokinins

20
Q
A
21
Q

Ethylene

A
  • effects: chlorosis, leaf abscission, stimulation of adventitious roots, and fruit ripening.
  • increases permeability of cell membranes
  • eg. Fruits infected with Ralstonia have proportional increase in ethylene. In verticillium wilt of tomato, ethylene presence at time of infection inhibits disease development whereas after infection, it increases disease
22
Q

IMPORTANT

Polysaccharides

A

Mucilaginous substances produced by pathogen propagules. Important in wilt diseases where they cause blockage of xylem and vascular bundles.