Topic 1: How do pathogen/pest populations respond to deployment of host resistance?
Topic 1: How do pathogen/pest populations respond to deployment of host resistance?
How do pathogen populations evolve in response to quantitative resistance?
How do pathogen populations evolve in response to quantitative resistance?
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Potato cyst nematodes (Globodera pallida) reared several generations on PR potato cultivars had increased reproductive rate, those on S cultivars did not (Schouten and Beniers, 1997, Phytopathology, 87:862-867).
Cowger and Mundt, 2002, Aggressiveness of Mycosphaerella graminicola isolates from susceptible and partially resistant wheat cultivars, Phytopathology 92:624-630
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Zhan et al (2002, Local adaptation and effect of host genotype on the rate of pathogen evolution: an experimental test in a plant pathosystem. J. Evol. Biol. 15:637-647)
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Bottom line on partial resistance
Topic 1: How do pathogen/pest populations respond to deployment of host resistance?
Host-selective toxins (HSTs)
How do fungal pathogen populations evolve in response to host resistance when HSTs are central to pathogenesis?
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HC-toxin detoxified directly by maize HM1, which encodes HC-toxin reductase (Sindhu et al, 2008, PNAS 105:1762-1767)
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Same ToxA gene present in Pyrenophora tritici-repentis (Ptr, cause of tan spot of wheat) and in Phaeosphaeria nodorum; high homology between ToxA genes
HSTs may be under diversifying selection
Types of natural selection
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Fig. 3. P. nodorum SnToxA parsimonious haplotype network of 123 P. n. isolates
Evidence for diversifying selection in SnToxA
P. nodorum has at least 4 HSTs (Friesen et al, 2008, Plant Physiology 146:682-693)
Why does wheat have genes for sensitivity to ToxA, etc.?
Conclusions on SnToxA – evolution of a small-protein HST
What drives evolution of a secondary metabolite cluster and can we expect rapid appearance of new specificities as in P. nodorum SnTox series?
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Resistance to HSTs
Conclusions for resistance breeding and resistance management where HSTs are involved