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in specific virulence genes are usually called races. The races present in any one season or in a particular locality may be identified by their behavior on a selection of cultivars carrying different combinations of genes conferring resistance. A hypothetical interaction between several races of a pathogen and a differential set of host cultivars is shown in Table 2.3.

Host Pathogen
Race 1 Race 2 Race 3 Race 4
Cultivar 1 +
Cultivar 2 +
Cultivar 3 +
Cultivar 4 +

      + = compatible disease reaction (host susceptible, pathogen virulent).

      − = incompatible disease reaction (host resistant, pathogen avirulent).

Image described by caption and surrounding text.

      More recent analysis of mechanisms of pathogenicity in some necrotrophic fungi has shown that host susceptibility can in some cases be determined by the interaction of a pathogen toxin with a plant receptor causing sensitivity to this toxin. In such cases, susceptibility is the dominant trait, and the interaction has been described as an “inverse gene‐for‐gene” model (see Chapter 10, Figure 10.10).

      The gene‐for‐gene theory has important practical implications. The sequential introduction of new host cultivars which differ in resistance genes has been accompanied by corresponding changes in pathogen populations, whereby new races have successively come to predominate. The implications of this will be discussed further in Chapter 12. The gene‐for‐gene theory is also an important starting point for molecular models of host–pathogen specificity. Where single genes determine the outcome of a particular interaction, identification of the gene products involved should clarify how host–pathogen recognition occurs. Progress toward this goal is described in Chapter 10.

      Books

      1 Nash, A., Dalziel, R., and Fitzgerald, J. (2015). Mims Pathogenesis of Infectious Disease. Washington, DC: Academic Press.

      2 Smith, S.E. and Read, D.J. (2010). Mycorrhizal Symbiosis, 3e. Washington, DC: Academic Press.

      Articles

      1 Andrivon, D. (1993). Nomenclature for pathogenicity and virulence: the need for precision. Phytopathology 83: 889–890. (and subsequent correspondence. See Phytopathology 85: 518–519, 1995).

      2 Cooke, R.C. and Whipps, J.M. (1980). The evolution of modes of nutrition in fungi parasitic on terrestrial plants. Biological Reviews 55: 341–362.

      3 Crute, I.R. (1994). Gene‐for‐gene recognition in plant‐pathogen interactions. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences 346: 345–349.

      4 Delaye, L., García‐Guzmán, G., and Heil, M. (2013). Endophytes versus biotrophic and necrotrophic pathogens – are fungal lifestyles evolutionarily stable traits? Fungal Diversity 60 (1): 125–135. https://doi.org/10.1007/s13225‐013‐0240‐y.

      5  Hartung, J.S., Beretta, J., Brinasky, R.H. et al. (1994). Citrus variegated chlorosis bacterium: axenic culture, pathogenicity, and serological relationships with other strains of Xylella fastidiosa. Phytopathology 84: 591–597.

      6 Kabbage, M., Yarden, O., and Dickman, M.B. (2015). Pathogenic attributes of Sclerotinia sclerotiorum: switching from a biotrophic to necrotrophic lifestyle. Plant Science 233: 53–60. https://doi.org/10.1016/j.plantsci.2014.12.018.

      7 Pariaud, B., Ravigné, V., Halkett, F. et al. (2009). Aggressiveness and its role in the adaptation of plant pathogens. Plant Pathology 58: 409–424.

      8 Simpson, A.J.G., Reinach, F.C., Arruda, P. et al. (2000). The genome sequence of the plant pathogen Xylella fastidiosa. Nature 406 (6792): 151–157.

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