Susceptibility toPhytophthora ramorumin a key infectious host: landscape variation in host genotype, host phenotype, and environmental factors

Abstract

Summary Sudden oak death is an emerging forest disease caused by the invasive pathogen Phytophthora ramorum. Genetic and environmental factors affecting susceptibility to P. ramorum in the key inoculum‐producing host tree Umbellularia californica (bay laurel) were examined across a heterogeneous landscape in California, USA. Laboratory susceptibility trials were conducted on detached leaves and assessed field disease levels for 97 host trees from 12 225‐m2 plots. Genotype and phenotype characteristics were assessed for each tree. Effects of plot‐level environmental conditions (understory microclimate, amount of solar radiation and topographic moisture potential) on disease expression were also evaluated. Susceptibility varied significantly among U. californica trees, with a fivefold difference in leaf lesion size. Lesion size was positively related to leaf area, but not to other phenotypic traits or to field disease level. Genetic diversity was structured at three spatial scales, but primarily among individuals within plots. Lesion size was significantly related to amplified fragment length polymorphism (AFLP) markers, but local environment explained most variation in field disease level. Thus, substantial genetic variation in susceptibility to P. ramorum occurs in its principal foliar host U. californica, but local environment mediates expression of susceptibility in nature.

Will all the trees fall? Variable resistance to an introduced forest disease in a highly susceptible host

“…Dodd et al (2005) did not find a relationship between any AFLP markers (whose greater number alone makes finding links more likely) or genetic distance between populations and resistance to ramorum blight in Q. agrifolia. Anacker et al (2008) did find AFLP markers associated with variation in susceptibility in U. californica; nevertheless, in the same study the authors inferred environment to have an even greater effect. Among-population differentiation was not significantly different in observed quantitative disease resistance (P ST ) than in neutral genetic markers (F ST ), so we cannot reject the null model that populations are not differentiated in phenotype beyond random variation (Felsenstein, 1986;Lande, 1992;Spitze, 1993).…”

“…Under-bark inoculations of branches detached from Quercus species have been used to assess variation in resistance to ramorum blight (Dodd et al, 2005;Dodd et al, 2008b;Hüberli et al, 2006a), but in tanoaks this method frequently yields nearly invisible lesions and large measurement error, precluding its use on a large scale (Hayden and Garbelotto, unpublished data). Detached-leaf inoculations with zoospore suspensions, both wounding and nonwounding, have been used to gauge host resistance to P. ramorum in its foliar hosts (Anacker et al, 2008;De Dobbelaere et al, 2010;Grünwald et al, 2008;Hüberli et al, 2006a). But tanoak leaves, again, often develop asymptomatic infections from zoospore solutions (Hansen et al, 2005).…”

Apparent competition in canopy trees determined by pathogen transmission rather than susceptibility

“…In central California, presence of bay laurel is associated with higher risk of pathogen establishment (Maloney et al 2005, Meentemeyer et al 2008a, with additional local-scale variation in pathogen dynamics driven by variations in forest microclimate (Meentemeyer et al 2008b) and bay laurel genotype (Anacker et al 2008). An analogous community dependency on pathogen transmission is known from Lyme disease Keesing 2000, LoGiudice et al 2003); communities with increased densities of the most competent reservoir host (white-footed mouse, Peromyscus leucopus) increased the prevalence of infectious vectors (black-legged tick, Ixodes scapularis).…”

Sudden Oak Death: Interactions of the Exotic Oomycete Phytophthora ramorum with Naïve North American Hosts

“…Although this variability seems to be regulated both genetically and by the environment (1,65), it is measurable and has a significant impact on disease levels. Where bay laurel populations are most resistant, tanoaks appear to be the primary and necessary infectious host; where populations are most susceptible, it appears that high bay laurel susceptibility may lead to high disease incidence even where climatic conditions are not ideal for the spread of SOD (65).…”