Qualitative Disease Resistance

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Qualitative Disease Resistance

• aka Vertical Qualitative Inoculum-reducing
  Major-effect Hypersensitive Monogenic R
  gene.Complete Race-specific Single gene
  Vertical Gene-for-gene

100 severity
Amount of disease
0 severity
Race 4
Race 3
Race 2
Race 1

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Quantitative Disease Resistance

• aka Horizontal Rate-reducing Minor-effect
  General Polygenic Additive Incomplete, Partial
  Race-nonspecific Multi-genic

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• Biotrophic pathogens
• Derive nutrition from living host cells, Usually
  establish a long-term interaction with the plant.
• Necrotrophic pathogens
• Kill host cells. Derive nutrition from dead cells

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The Molecular Basis of Qualitative/Major gene
resistancea chronological summary
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1940s
H. H. Flor
MOLECULAR PLANT PATHOLOGY 8 349364
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Pathogen
Host
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Pathogen
avr1avr2
avr1AVR2
AVR1avr2
AVR1AVR2
 
Compatible (Susceptible)
Incompatible (Resistant)
Incompatible (Resistant)
Incompatible (Resistant)
R1-R2-
 Compatible (Susceptible)
Compatible (Susceptible)
Incompatible (Resistant)
 Incompatible (Resistant)
 R1-r2r2
Host
Compatible (Susceptible)
 Incompatible (Resistant)
Compatible (Susceptible)
 Incompatible (Resistant)
r1r1R2-
Compatible (Susceptible)
Compatible (Susceptible)
Compatible (Susceptible)
Compatible (Susceptible)
r1r1r2r2
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What does this mean?

• Implies, interaction (direct of otherwise) of
  dominant Resistance and Avirulence gene products
  leads to resistance.
• The loss of an AVR gene in the pathogen can
  render the corresponding R gene essentially
  useless.
• It doesnt matter how many interactions there are
  leading to compatibility. A single R/Avr match
  will lead to resistance.

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What did classical genetics tell us?

• Gene-for-gene interactions were identified in
  many different interactions with many different
  types of pathogens
• R-genes were often clustered in complex loci.
• Avr genes were not clustered
• What does this suggest to you?

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Predictions

• Pathogen is trying to lose Avr genes.
• Why does a pathogen have AVR genes in the first
  place?
• Host is trying to develop new types of R genes

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What was known about R-genes?

• Often associated with hypersensitive response
  (HR)
• In some cases, usually where complex loci are
  involved, they were quite unstable.

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Three elegant studies

• Confirms our understanding of Gene-for-Gene
• Helps us understand R-gene structure and
  variability
• Helps us understand R-gene function

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Elicitors from the Cladosporium fulvum/ tomato
system

• Pierre de Wit
• Several Avr/R gene interactions were
  characterized
• Avr2/Cf2
• Avr4/Cf4
• Avr5/Cf5
• Avr9/Cf9

http//www.php.wur.nl/UK/Research/Cladosporium/?wb
c_purposeBasicWBCMODEPresentationUnpublished/a
vr
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• Fungus grows strictly in the apoplastic space-
  doesnt invade host cells
• Can you isolate Avr elicitors from apoplastic
  fluid

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Cf2
Cf4
Isolate intercellular fluid and inject into Cf2,
Cf4, Cf5 Cf9 leaves
Cf5
Cf9
http//www.php.wur.nl/UK/Research/Cladosporium/
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Conclusions

• Identified specific elicitors associated with
  R-gene-mediated defense response.
• Specific peptide elicitors were identified from
  intercellular fluid
• Dont necessarily need pathogen itself to be
  present to invoke R-gene mediated resistance

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Unstable nature of R-genes

• Seems to be associated with meiosis
• R-genes dont spontaneously cease functioning in
  an existing plant.

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tester - no R gene
Homozygous for R gene, heterzygous for flanking
markers
A
a
a
A
Select susceptible progeny
r
X
r
OR
R
R
25/15,646
b
b
B
B
24/25 show non-parental combinations
Sudapak et al, 1993 Genetics, Vol 133, 119-125
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Sudapak et al, 1993 Genetics, Vol 133, 119-125
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Conclusion

• Complex nature of R-gene loci leads to their
  unstable nature.
• NB many , but not all, R-genes occur in complex
  loci.

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Cell Autonomous Nature of R-genes
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Developing maize embryos were exposed to X-rays
rp1
Rp1
rp1
oy
Oy
oy
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• HR in green sectors
• Pustules in yellow sectors
• HR doesnt cross into yellow sectors (much-1F).
• Rp1 is not diffusible