Gene-for-gene relationship

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The gene-for-gene relationship was discovered by H.H. Flor[1][2] who was working with rust (Melampsora lini) of flax (Linium usitatissiumum). Flor was the first scientist to study the genetics of both the host and parasite and to integrate them into one genetic systems.[3]

Flor showed that the inheritance of both resistance in the host and parasite ability in the parasite is controlled by pairs of matching genes. One is a plant gene called the resistance gene. The other is a parasite gene called the avirulence gene. If a host individual has several of these resistance genes, it is resistant to any parasite individual that lacks one or more of the matching genes for parasite ability. And it is susceptible to any parasite individual that has all (or more than all) of the matching genes.

Person[4] was the first scientist to study plant pathosytem ratios rather than genetics ratios in host-parasite systems. In doing so, he discovered the differential interaction that is common to all gene-for-gene relationships and that is now known as the Person differential interaction.[3]

Contents

[edit] Resistance Genes

[edit] Classes of Resistance Gene

There are several different classes of R Genes. The major class are the NBS-LRR genes. The protein product of these R genes contain a nucleotide binding site and a leucine rich repeat. Within this class of R genes are two subclasses: -

  • One subclass has an amino-terminal Toll/Interleukin 1 receptor homology region (TIR). This includes the N resistance gene of tobacco against TMV.
  • The other subclass does not contain a TIR and instead has a leucine zipper region at its amino terminal.

The protein products encoded by this class of resistance gene are located within the plant cell cytoplasm.

However there is an extracelluar LRR class of R genes, including rice Xa21 for resistance against Xanthamonas and the cf genes of tomato that confer resistance against [[C. fulvum]]. The proteins have classic receptor-kinase formats - an extracelluar LRR, a membrane spanning region and an intracellular protein kinase domain. The reasons that these particular R proteins have extracellular domains is that the pathogens they protect against have an extracellular lifestyle.

The Pseudomonas tomato resistance gene (Pto) belongs to a class of its own. It encodes a Ser/Thr kinase but has no LRR. It requires the prescence of a linked NBS-LRR gene, prf, for activity.

[edit] Specificity of Resistance Genes

R gene specificity (recognising certain Avr gene products) is believed to be conferred by the leucine rich repeats. LRRs are multiple, serial repeats of a motif of roughly 24 amino acids in length, with leucines or other hydrophobic residues at regular intervals. Some may also contain regularly spaced prolines and arginines.[5]

LRRs are involved in protein-protein interactions, and the greatest variation amognst resistance genes occurs in the LRR domain. LRR swapping experiments between resistance genes in flax rust resulted in the specificity of the resistanc gene for the avirulence gene changing.[6]

[edit] Recessive Resistance Genes

Most resistance genes are autosomal dominant but there are some, most notibly the mlo gene in barley, in which monogenic resistance in conferred by recessive alleles. mlo protects barley against nearly all pathovars of powedery mildew.

[edit] Avirulence Genes

There is no common structure between Avirulence genes, except that most are secreted proteins. Because there would be no evolutionary advantage to a pathogen keeping a protein that only serves to have it recognised by the plant, it is believed that the products of Avr genes, sometimes known as effector proteins, play an important role in virulence in genetically susceptible hosts.

They are probably targets of proteins involved in plant innate immunity, as homologues of Avr genes in animal pathogens have been shown to do this. The AvrBs3 family of proteins possess DNA binding domains, nuclear localisation signals and acidic activation domains and are believed to function by altering host cell transcription.[7]

[edit] The Guard Hypothesis

It was originally believed that gene-for-gene resistance was conferred by a direct interaction between the R gene product and the Avr gene product, but experiments failed to show this. This lack of eveidence for a direct interaction led to the formation of the guard hypothesis.

This model proposes that the R proteins interact, or guard, a protein known as the guardee which is the target of the Avr protein. When it detects interference with the guardee protein, it activates resistance.

Several experiments support this hypothesis. Yeast two-hybrid studies of the tomato Pto/Prf/AvrPto interaction showed that the Avirulence protein, AvrPto, interacted directly with Pto despite Pto not having an LRR. This makes Pto the guardee protein, which is protected by the NBS-LRR protein Prf.

Further support for the guard hypothesis comes from the Rpm1 gene in Arabidopsis. This R gene product is able to respond to two completely unrelated Avirulence factors from P. syringae. The guardee protein is RIN4, which is hyperphosphorylated by the Avr proteins.

[edit] References

  1. ^ Flor H.H. (1942) Inheritance of pathogenicity in Melampsora lini. Phytopath. 32:653-669
  2. ^ Flor H.H. (1947) Inheritance of reaction to rust in flax. J. Agric. Res., 74:241-262
  3. ^ a b Robinson, Raoul A. (1987) Host Management in Crop Pathosystems, Macmillan Publishing Company
  4. ^ Person, C.O. (1959) Gene-for-gene relationships in parasitic systems. Can. J. Bot., 37:1101-1130.
  5. ^ Dickinson, M. Molecular Plant Pathology, 2003.
  6. ^ Brody J DeYoung & Roger W Innes. Plant NBS-LRR proteins in pathogen sensing and host defense. Nature Immunology 2006. Volume 7, pages 1243-1249.
  7. ^ Lahaye, Thomas and Bonas, Ulla. Molecular Secrets of bacterial Type III effector proteins. Trends in Plant Science, 2001. Volume 6, issue 10, pages 479-485
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