GENE-FOR-GENE INTERACTIONS

 

For Necrotrophs:  Pathogen virulence is dominant because of the need to produce a functional toxin and/or enzyme, whereas avirulence, the inability to cause disease, is inherited as a recessive trait.

 

R gene –

“anti-dote”
 
Oval: ENZ
 

 

 

Oval: ENZ

Disease
 
 

 

 

 


The first R gene to be isolated was Hm1 from maize, which confers resistance to the leaf spot fungus Cochliobolus carbonum.

 

 Hm1 codes for a reductase enzyme that detoxifies the C. carbonum HC-toxin. This toxin inhibits histone deacetylase activity  and the Hm1 gene product is thought to inactivate the toxin.

 

 

Resistance to Biotrophs – avirulence and resistance are usually genetically dominant traits.

 

More than 20 resistance genes have been cloned which fall into five main classes.

 

(i)              Detoxifying enzymes – e.g. Hm1.

(ii)           Intracellular protein kinases (Pto)- serine/threonine protein kinases

 

(iii)        Intracellular Leucine Rich repeats.

 

LxxLxxLxxLxLxx(N/C/T)c)x) Lxx/Pxx

 

Implicated in protein/protein interactions.

 

Cf-9 – 23 repeats

Cf-4 – 21 repeats

Cf-2 – 37 repeats

 

Mutated RPP5 LRR – abolished Multiple R-gene functions –

 

Avr –interacting region? But where is the specificity?

 

(iiia) With Nucleotide binding site (NBS) and with Leucine Zipper

 

NBS – founding in numerous ATP/GTP binding proteins.

Consists of

-         GPGGVGKT- (P-loop)

-         Asparate necessary to co-oridinate metal io for phosphate transfer.

-         Arginine to interact with purine base of ATP. BUT no biochemical evidence.

 

 

 

Leucine Zipper – XDLXXX promotes either dimerisation or specific interaction with other proteins.

(iiib)With Nucleotide binding site (NBS) with homology to a domain Toll (insect) and IL-1 receptor (human) receptor.  – TIR region.

 

Significance of this is unknown

 

(iv)         Membrane –associated / extracellular protein.

 

 

(v)            Kinase with extracellular Leucine-rich repeats.

 

How do R and avr gene products interact?

 

Only with Pto has been shown to directly interact with the avrPto.

 

BUT Pto needs to interact with Prf-  a Leucine rich protein to function.

 

Is this a model for resistance gene function – The Modular Model?

 

 

 

THIRD HANDOUT: New developments in our under standing of gene-for-gene interaction.

 

The “Guard” hypothesis. The RIN4 story

(De Wit 2002, 416, 810-803)

 

 

·       RIN4 = RPM1-interacting protein 4

·       First identified based on its interaction with avrRpm1-

Isolated by co-precipitation.

·       AvrRpm1 induces the phosphorylation of RIN4.

·       RIN4 suppresses defence gene expression

 


 

 

 

 

 

 

 

 

 

 

 

·       AvrRpm1 interaction further enhances its suppressive effects.

·       BUT RIN4 is required for RPM1 resistance to bacteria

·       and other R genes too!!..avrRpt2 interaction with RPS2.

·       Hence, RIN4 is a switch…..and RPM1 “guards” its ability to switch to the resistant response.  

 

References

 

de Wit, P. J. (2002). “Plant biology: on guard.” Nature 416(6883): 801-3.

         

Mackey et al.,. (2003). Cell 112(3): 379-89.

 

Mackey et al.,. (2002). Cell 108(6): 743-54.