The Coevolutionary Implications of Host Tolerance

Best, Alex; White, Andrew; Boots, Mike

doi:10.1111/evo.12368

Cited by 74 publications

(86 citation statements)

References 46 publications

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“…Invasion, infection, or pathogen growth -each a scale-dependent process -can determine pathogen impacts such as loss of growth and mortality. In contrast, persistence can result from a combination of factors including survival as a saprotroph, a broad host range (generalism) combined with tolerance (host amelioration of negative impacts) in some hosts (Best et al 2014), and/or formation of long-lived survival structures (Smith et al 2006). Disease destructiveness and persistence may interact in evolutionary and ecologically complex ways such as diseases that are persistent but not destructive, destructive but not persistent, and most consequentially, destructive and persistent disease.…”

Section: Introductionmentioning

confidence: 99%

Resiliency or restoration: management of sudden oak death before and after outbreak

et al. 2017

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Forests at risk to diseases caused by invasive Phytophthora pathogens can be grouped into two broad classes: those already invaded by the focal pathogen where disease has emerged or those at significant risk of invasion and subsequent emergence of disease. This dichotomy represents distinct management scenarios -treating after or before disease emerges -with a set of epidemiological, ecological, and practical management characteristics that determine optimal actions and associated costs. Here we present the initial outcomes from two management experiments aimed at restoring forest structure or protecting against changes to forest structure following invasion of Phytophthora ramorum, the cause of sudden oak death (SOD). We conducted a stand-level restoration experiment on Mount Tamalpais (Marin County, CA) at three sites where the disease has killed most overstory tanoak and dramatically increased understory vegetation density and fuels. A separate experiment in an uninvaded, at risk forest was conducted near Lacks Creek, in Humboldt County. This treatment is an attempt to increase forest resiliency to catastrophic loss of tanoak, increased fuels associated with tree mortality, and densification of the understory that are expected to accompany disease in these stands within the coming decade. Restoration experiments employed two types of mastication of understory vegetation and hand-crew thinning with pile burning; resiliency experiments employed hand crews. Treatments were compared to a set of reference conditions representing overly dense stands where intervention is needed and extensively managed stands that serve as management targets. Both restoration and resiliency treatments greatly reduced density of key sporulation supporting hosts with modest-to-minimal effects on stand basal area. Prior land use, especially past harvesting, was a primary factor determining treatment costs and potential disease impacts in treated vs untreated stands. Although both restoration and resiliency management strategies are likely to reduce disease impacts, treatment costs vary substantially and will greatly influence when and where each approach is optimal.

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Section: Introductionmentioning

confidence: 99%

Resiliency or restoration: management of sudden oak death before and after outbreak

et al. 2017

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“…serves as a concise metaphor for the selection pressures on hosts to constantly change defense mechanisms against pathogens and the counterselection on the pathogens for continuously developing means for overcoming such evolving defenses, resulting in the appearance of both organisms "running in place" (1). Variations of the Red Queen as well as alternative theories, most unified around the centrality of biotic interactions as a driving force, have been proposed as explanations for (i) taxon extinction [Van Valen's original Red Queen's hypothesis (2)]; (ii) the evolution and maintenance of sex, genetic recombination, and immune systems (3)(4)(5); (iii) as a framework for understanding invasions of exotic species (6); and (iv) as mechanism(s) selecting for hostpathogen coevolution [i.e., broad versus specific host ranges and/or host tolerance (7)(8)(9)]. …”

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confidence: 99%

Tenebrionid secretions and a fungal benzoquinone oxidoreductase form competing components of an arms race between a host and pathogen

Pedrini

Ortiz‐Urquiza

Huarte‐Bonnet

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

123

118

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Entomopathogenic fungi and their insect hosts represent a model system for examining invertebrate-pathogen coevolutionary selection processes. Here we report the characterization of competing components of an arms race consisting of insect protective antimicrobial compounds and evolving fungal mechanisms of detoxification. The insect pathogenic fungus Beauveria bassiana has a remarkably wide host range; however, some insects are resistant to fungal infection. Among resistant insects is the tenebrionid beetle Tribolium castaneum that produces benzoquinone-containing defensive secretions. Reduced fungal germination and growth was seen in media containing T. castaneum dichloromethane extracts or synthetic benzoquinone. In response to benzoquinone exposure, the fungus expresses a 1,4-benzoquinone oxidoreductase, BbbqrA, induced >40-fold. Gene knockout mutants (ΔBbbqrA) showed increased growth inhibition, whereas B. bassiana overexpressing BbbqrA (Bb::BbbqrAO) displayed increased resistance to benzoquinone compared with wild type. Increased benzoquinone reductase activity was detected in wild-type cells exposed to benzoquinone and in the overexpression strain. Heterologous expression and purification of BbBqrA in Escherichia coli confirmed NAD(P)H-dependent benzoquinone reductase activity. The ΔBbbqrA strain showed decreased virulence toward T. castaneum, whereas overexpression of BbbqrA increased mortality versus T. castaneum. No change in virulence was seen for the ΔBbbqrA or Bb::BbbqrAO strains when tested against the greater wax moth Galleria mellonella or the beetle Sitophilus oryzae, neither of which produce significant amounts of cuticular quinones. The observation that artificial overexpression of BbbqrA results in increased virulence only toward quinone-secreting insects implies the lack of strong selection or current failure of B. bassiana to counteradapt to this particular host defense throughout evolution.

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“…The crucial difference is that resistance reduces the risk of infection and/or the replication rate of the parasite in the host, whereas tolerance does not (but note that tolerance can still impose selection on the parasite [3]). It is important to distinguish between resistance and tolerance because these two types of defence lead to different ecological and evolutionary interactions between hosts and their parasites [3]–[6]. For example, if hosts evolve resistance, this should reduce the prevalence of the parasite in the host population.…”

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confidence: 99%