Monday, August 2, 2010

PS 12-98: Explaining variation in host tolerance of infectious disease

James P. Cronin1, Miranda E. Welsh1, Martin G. Dekkers1, Samuel T. Abercrombie1, and Charles E. Mitchell2. (1) University of North Carolina at Chapel Hill, (2) University of North Carolina

Background/Question/Methods

Research suggests that vectored, generalist pathogens can influence host community structure. Consequently, predicting host tolerance to infection is an important ecological goal.  We hypothesize that host tolerance is causally determined by a few, general host physiological traits. Plant phenotypes can be mapped onto a continuum that represents a rapid resource acquisition - resource conservation trade-off. At one end are quick return (QR) phenotypes, which have short-lived leaves with high photosynthetic capacity (Amax), tissue nitrogen concentration (TN), and specific leaf area (SLA). At the other end, are slow return (SR) phenotypes, which have long-lived leaves of low Amax, TN, and SLA.  Relationships between host phenotypes and tolerance of herbivory are better known: QRs are generally tolerant of herbivory (i.e., damage to cheap, high resource return tissue is not extremely costly) while SRs are generally intolerant of herbivory (i.e., damage to expensive, low resource return tissue is costly). Direct tests linking QR-SR phenotypic gradients to tolerance of disease, however, are lacking. We therefore predicted our host species phenotypes would vary along the SR-QR continuum and that host tolerance would be greatest on QR phenotypes. We further predicted the SR-QR continuum would provide a better explanation compared to other factors, namely phenotypic plasticity, phylogeny, lifespan, and provenance.  We conducted controlled greenhouse experiments using six California grass species and an aphid vectored generalist plant pathogen (barley yellow dwarf virus PAV; BYDV). We quantified host phenotypes and conducted experimental BYDV inoculations using aphid vectors.  
Results/Conclusions

Our species fell along a QR-SR continuum. BYDV impact on total mass did not vary by species, although infection significantly reduced total mass by thirty percent. Variation in BYDV impact on total plant mass was not explained by host physiological phenotype, phenotypic plasticity, phylogeny, lifespan, or provenance. In contrast, BYDV impact on root mass ratio varied amongst species, ranging from zero to forty-five percent reduction of root mass ratio. BYDV impact on root mass ratio was explained by phylogeny, lifespan, and provenance, not host physiological phenotype or phenotypic plasticity. Annuals experienced a nineteen percent greater reduction of root mass ratio compared to perennials. These results suggest that tolerance is explained by traits unrelated to the QR-SR continuum or plasticity and that covary with phylogenetic group, lifespan, or provenance.