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Related Experiment Videos

Specificity versus detectable polymorphism in host-parasite genetics

S A Frank1

  • 1Department of Ecology and Evolutionary Biology, University of California, Irvine 92717.

Proceedings. Biological Sciences
|December 22, 1993
PubMed
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Detectable host resistance and parasite host range polymorphism can mislead interpretations of host-parasite interactions. Analyzing a simple haploid model reveals that observed patterns may fit multiple specificity models, complicating evolutionary and biochemical analyses.

Area of Science:

  • Evolutionary biology
  • Population genetics
  • Host-parasite interactions

Background:

  • Host resistance and parasite host range polymorphism are often used to infer specificity in host-parasite interactions.
  • Current models, like the gene-for-gene specificity, are commonly observed in plant-pathogen systems.
  • The biochemical elicitor-receptor model is frequently used to explain plant-pathogen recognition.

Purpose of the Study:

  • To analyze a simple haploid model to demonstrate that detectable polymorphism is a poor guide to host-parasite specificity.
  • To illustrate how matching-allele specificity can be mistaken for gene-for-gene specificity.
  • To highlight the need for comparing data with multiple theoretical models and considering population genetic consequences of biochemical models.

Main Methods:

Related Experiment Videos

  • Analysis of a simple haploid model assuming matching-allele specificity.
  • Comparison of fitness assumptions required for matching-allele versus gene-for-gene specificity.
  • Evaluation of the compatibility of the elicitor-receptor model with both specificity types.

Main Results:

  • Detectable polymorphism in a matching-allele system can lead to the inference of gene-for-gene specificity.
  • Both gene-for-gene and matching-allele models can be constructed to fit available data.
  • The elicitor-receptor model is consistent with both gene-for-gene and matching-allele specificity.

Conclusions:

  • Observed polymorphism alone is insufficient to reconstruct both specificity and population history.
  • Inferred specificity and polymorphism require comparison with a family of theoretical models.
  • Biochemical models of specificity must be validated by their population genetic implications.