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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 1. Race 2. Race 3. Race 4.

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qualitative disease resistance
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 1

Race 2

Race 3

Race 4

Balint-Kurti lecture 1

quantitative disease resistance
Quantitative Disease Resistance

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

Balint-Kurti lecture 1

slide7
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

Balint-Kurti lecture 1

the molecular basis of qualitative major gene resistance a chronological summary
The Molecular Basis of Qualitative/Major gene resistancea chronological summary

Balint-Kurti lecture 1

slide9

1940’s

H. H. Flor

Balint-Kurti lecture 1

MOLECULAR PLANT PATHOLOGY 8 349–364

slide10

Pathogen

Host

Balint-Kurti lecture 1

slide11

Pathogen

AVR1AVR2

AVR1avr2

avr1AVR2

avr1avr2

R1-R2-

Incompatible

(Resistant)

Incompatible

(Resistant)

Incompatible

(Resistant)

Compatible

(Susceptible)

 R1-r2r2

 Incompatible

(Resistant)

Incompatible

(Resistant)

Compatible

(Susceptible)

 Compatible

(Susceptible)

Host

r1r1R2-

 Incompatible

(Resistant)

Compatible

(Susceptible)

 Incompatible

(Resistant)

Compatible

(Susceptible)

r1r1r2r2

Compatible

(Susceptible)

Compatible

(Susceptible)

Compatible

(Susceptible)

Compatible

(Susceptible)

Balint-Kurti lecture 1

what does this mean
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 doesn’t matter how many interactions there are leading to compatibility. A single R/Avr match will lead to resistance.

Balint-Kurti lecture 1

what did classical genetics tell us
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?

Balint-Kurti lecture 1

predictions
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

Balint-Kurti lecture 1

what was known about r genes
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.

Balint-Kurti lecture 1

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

Balint-Kurti lecture 1

elicitors from the cladosporium fulvum tomato system
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/?wbc_purpose=Basic&WBCMODE=PresentationUnpublished/#avr

Balint-Kurti lecture 1

slide18

Fungus grows strictly in the apoplastic space- doesn’t invade host cells

  • Can you isolate Avr elicitors from apoplastic fluid

Balint-Kurti lecture 1

slide19

Cf2

Cf4

Isolate intercellular fluid and inject into Cf2, Cf4, Cf5 Cf9 leaves

Cf5

Cf9

http://www.php.wur.nl/UK/Research/Cladosporium/

Balint-Kurti lecture 1

conclusions
Conclusions
  • Identified specific elicitors associated with R-gene-mediated defense response.
    • Specific peptide elicitors were identified from intercellular fluid
  • Don’t necessarily need pathogen itself to be present to invoke R-gene mediated resistance

Balint-Kurti lecture 1

unstable nature of r genes
Unstable nature of R-genes
  • Seems to be associated with meiosis
    • R-genes don’t spontaneously cease functioning in an existing plant.

Balint-Kurti lecture 1

slide23

“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

Balint-Kurti lecture 1

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

Balint-Kurti lecture 1

cell autonomous nature of r genes
Cell Autonomous Nature of R-genes

Balint-Kurti lecture 1

slide27

Developing maize embryo’s were exposed to X-rays

rp1

Rp1

rp1

oy

Oy

oy

Balint-Kurti lecture 1

slide28
HR in green sectors
  • Pustules in yellow sectors
  • HR doesn’t cross into yellow sectors (much-1F).
  • Rp1 is not diffusible

Balint-Kurti lecture 1