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‡ Land plants are attacked by:


± Herbivores (insects, mammals, etc.)
± Pathogens
Pathogen Strategies
1. Necrotrophic ± plant tissue killed and then colonized;
broad host range
e.g., rotting bacteria (V )

2. Biotrophic ± plant cells remain alive, narrow host range


(1 plant species)
e.g., viruses, nematodes, fungal mildews

3. Hemibiotrophic ± biotrophic phase, then necrotrophic,


intermediate host range
e.g., 
  (potato blight disease)

ajor Pathogens
1) Viruses - most are RNA viruses
Have a small compact genome which encodes:
coat protein
RNA-dependent RNA polymerase (for replication)
movement protein(s)

Some plant RNA viruses also encode:


protease for processing polyprotein (Potyvirus)
capping enzyme
RNA helicase

Some also exist as multiple particles, and a segmented


RNA genome (e.g., Bromoviruses, 3 particles needed for
infection).
An encapsulated SS
RNA virus: Tobacco
mosaic virus

DS DNA virus,
Cauliflower
osaic Virus

Fig. 21.10, Buchanan et al.


Genome of Cauliflower
osaic
Virus (Ca
V)

Fig. 21.11 , Buchanan et al.


1a) Viroids- naked RNA infectious
agents

‡ Single strands of RNA


‡ Lack the protein coat of viruses
‡ Do not code for any specific protein
‡ Replicate in the nuclei of infected cells
e.g., Potato spindle tuber viroid was the
first to be identified.
Viroid structure
2) Bacteria
3) Fungi - plant pathogens found among 4
major groups
4) Nematodes - major root parasites, also
increase infection by microorganisms

Insects and other herbivores can also


transmit plant diseases.
Distribution of Oak Wilt in the US
ð  

 

Ö  

  

odes of Transmission of Oak Wilt fungus

K     


Plant Defenses
1) Physical barriers: cuticle, thorns, cell walls

2) Constitutively produced chemicals (e.g., phytoalexins)


and proteins (e.g., Ricin)

1 and 2 together provide ³non-host resistance´ against


most potential pathogens. However, some pathogens
get around these protections (but only for certain plants),
and generate induced responses, which work to limit the
disease.

3) Induced responses
Plant Defense Response
Compatible interaction w disease
Incompatible interaction w resistance

3 aspects of response:
1. Hypersensitive
2. Local
3. Systemic
Hypersensitive response
‡ Rapid - within 24 h
‡ Not always needed for resistance
‡ Includes:
± oxidative reactions (production of hydrogen
peroxide)
± deposition of callose (related to cellulose)
± opening of ion channels
± apoptosis (programmed cell death)
Disease symptoms
(necrotic lesions
surrounded by
chlorosis) caused by
the phytobacterium
    
  
  
  strain DC3000
on inoculated leaves
of a susceptible
 
 
Col-0 plant. Green
leaves were not
inoculated. [Photo by
R. Thilmony]
Local responses
‡ Cessation of cell cycle
‡ Induction of genes that promote resistance
± Phenylpropanoid pathway induced: products include
salicylic acid (secondary inducer: induces other
pathogenesis-related proteins), lignins (cell wall), and
flavonoids
± Pathogenesis-related (PR) proteins
± Phytoalexins increased
‡ Fortification of cell walls with lignin,
hydroxyproline-rich glycoproteins (HRGPs), etc.
Systemic Response or Systemic
Acquired Resistance (SAR)

‡ SAR takes 24-48 h to start, can last for months

Involves gene activation and a transmitted signal.


‡ Genes induced:
chitinases
ȕ 1,3- glucanases
other PR proteins
Signaling Cascade for Defense
Responses
‡
olecular nature of   :
1. Cell wall proteins (e.g., Harpin)
2. Intracellular proteins (defined genetically
in a bacterium by cloning avirulent
loci)
3. Peptide derived from a larger protein
(from a fungus)
4. Heptaglucan (small oligosaccharide)
Secondary Signals (3)
1. Ca+2 , required for subsequent steps

ay mediate phosphorylation-dephos. events
involved in transcriptional or post-
transcriptional gene regulation (there are a
number of genes whose transcription
increases, and some decrease)

‡ Some defense genes also induced by


blue-UV light or other stresses
2. H2O2 (hydrogen peroxide)

‡ Plays multiple roles:


± induces defense-related genes
± induces apoptosis
± causes cross-linking of cell wall proteins
(more resistant to wall-degrading enzymes)
± may directly kill pathogens
3. Salicylic acid
‡ required for SAR
‡ levels increase locally and at distance
from infection
‡ Systemic Signal? Probably not. Still
unknown.

odel derived
mostly from
studies in cell
culture using
specific elicitors.
However, there is
evidence for
induction in inact
plants by `
genes. Some
aspects are also
constitutive and
help block most
microbes (non-
host resistance).

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