Host-Pathogen Dynamics in Experimental Populations of Silene Alba and Ustilago Violacea. II. Experimental Tests of Theoretical Models

Thrall, Peter H.; Jarosz, A. M.

doi:10.2307/2261264

Cited by 77 publications

(55 citation statements)

References 22 publications

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“…Most metapopulation models concentrate on the role that extinction and recolonization play in stabilizing coexistence and maintaining selected genetic variation in host and parasite (Frank, 1993;Ladle et al, 1993;Antonovics et al, 1994;Thrall & Jarosz, 1994a;Thrall & Jarosz, 1994b;Judson, 1995;Frank, 1996). Extinction/colonization processes of parasite and host in a metapopulation system depend on subpopulation size, the underlying genetic basis of the interaction between parasite and host, and the scale at which both players migrate between populations.…”

Section: Local Adaptation In a Metapopulation Contextmentioning

confidence: 99%

Local adaptation in host–parasite systems

1998

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In host-parasite coevolutionary arms races, parasites probably have an evolutionary advantage. Parasite populations should be locally adapted, having higher mean fitness on sympatric than allopatric hosts. Here we assess evidence for local parasite advantage. Further we investigate how adaptation and counter-adaptation of parasites and hosts, necessarily occurring in sympatry, can generate a pattern of local adaptation. Already simple frequency-dependent selection models generate complex patterns of parasite performance on sympatric and allopatric populations. In metapopulations, with extinction, recolonization, and gene flow, variable selection pressure and stochasticity may obscure local processes or change the level at which local adaptation occurs. Alternatively, gene flow may introduce adaptive variation, so differential migration rates can modify the asymmetry of host and parasite evolutionary rates. We conclude that local adaptation is an average phenomenon. Its detection requires adequate replication at the appropriate level, that at which the local processes occur.

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Section: Local Adaptation In a Metapopulation Contextmentioning

confidence: 99%

Local adaptation in host–parasite systems

1998

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“…Kaltz, unpubl. data; see also ) and this may explain higher mortality of infected plants in some years (Thrall and Jarosz 1994a;O. Kaltz, unpubl.…”

Section: Study Organismsmentioning

confidence: 90%

LOCAL MALADAPTATION IN THE ANTHER-SMUT FUNGUSMICROBOTRYUM VIOLACEUMTO ITS HOST PLANTSILENE LATIFOLIA: EVIDENCE FROM A CROSS-INOCULATION EXPERIMENT

et al. 1999

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Abstract.-Conventional wisdom holds that parasites evolve more rapidly than their hosts and are therefore locally adapted, that is, better at exploiting sympatric than allopatric hosts. We studied local adaptation in the insect-transmitted fungal pathogen Mierobotryum violaceum and its host plant Silene latifolia. Infection success was tested in sympatric (local) and allopatric (foreign) combinations of pathogen and host from 14 natural populations from a metapopulation. Seedlings from up to 10 seed families from each population were exposed to sporidial suspensions from each of four fungal strains derived from the same population, from a near-by population « 10 km distance), and from two populations at an intermediate « 30 km) and remote « 170 km) distance, respectively. We obtained significant pathogen X plant interactions in infection success (proportion of diseased plants) at both fungal population and strain level. There was an overall pattern of local maladaptation of this pathogen: average fungal infection success was significantly lower on sympatric hosts (mean proportion of diseased plants = 0.32 ± 0.03 SE) than on allopatric hosts (0.40 ± 0.02). Five of the 14 fungal populations showed no strong reduction in infection success on sympatric hosts, and three even tended to perform better on sympatric hosts. This pattern is consistent with models of time-lagged cycles predicting patterns of local adaptation in host-parasite systems to emerge only on average. Several factors may restrict the evolutionary potential of this pathogen relative to that of its host. First, a predominantly selfing breeding system may limit its ability to generate new virulence types by sexual recombination, whereas the obligately outcrossing host S. latifolia may profit from rearrangement of resistance alleles by random mating. Second, populations often harbor only a few infected individuals, so virulence variation may be further reduced by drift. Third, migration rates among host plant populations are much higher than among pathogen populations, possibly because pollinators prefer healthy over diseased plants. Migration among partly isolated populations may therefore introduce novel host plant resistance variants more often than novel parasite virulence variants. That migration contributes to the coevolutionary dynamics in this system is supported by the geographic pattern of infectivity. Infection success increased over the first lO-km range of host-pathogen population distances, which is likely the natural range of gene exchange.

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“…Researchers tend to define their research disciplines with labels (i.e., ecology, genetics), potentially impeding important research at the interface of disciplines. For example, at the population level, there are still few studies that truly integrate population dynamics and genetic variation (129), and community ecologists are just starting to add knowledge of phylogenetic relationships among hosts to our understanding of multispecies interactions (56). Similarly, ecosystem research in disease ecology must be done with recognition that plants and pathogens will likely evolve in response to a changing environment (38).…”

Section: Future Directionsmentioning

confidence: 99%

Disease in Natural Plant Populations, Communities, and Ecosystems: Insights into Ecological and Evolutionary Processes

Alexander

2010

Plant Disease

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Pathogens are associated with virtually all plant species, from a diverse array of habitats. Although we know the most about diseases of economically important plants, the goal of this article is to describe current work on host-pathogen interactions in natural or unmanaged systems outside of the crop field or forestry plantation. Agricultural scientists, of course, have contributed to this research. For example, disease resistance genes are often discovered as a result of surveys of wild relatives of crop plants, and it is well known that crop disease levels can be influenced by diseases in nearby weeds. Starting in the late 1970s, however, research on natural plant-pathogen interactions began to both increase and diversify, with an explicit goal of understanding the ecology and evolution of these interactions. This article will trace the history of this young discipline and provide highlights of ongoing research areas. I will focus on work by ecologists and evolutionary biologists that often is not published in plant pathology or forestry journals.A first step is to define a natural system as opposed to an agricultural or human-managed system. In contrast to most row crops, most natural populations occur in complex spatial arrangements with tens to hundreds of other species, are genetically diverse, and consist of plants of different ages and developmental stages. Seeds produced by a population in one year are the source of future generations at the site. Natural populations need not be pristine; as defined above, roadside weeds are as natural as prairie wildflowers. This natural versus agricultural dichotomy is also, of course, simplistic. Forest plantations and pasture landscapes have many natural attributes, and the degree of distinction between agricultural and natural ecosystems varies around the world.Although there have always been researchers intrigued by the role of pathogens in nature (58), publications in the 1970s and 1980s were influential in introducing the study of plant disease to ecologists and evolutionary biologists. For example, John Harper, a British biologist, published a landmark book in 1977 called Population Biology of Plants (61). This large tome (892 pages) encouraged ecologists to view plants not as vegetation, but as populations of individuals. One of his 17 chapters was titled "Pathogens" and emphasized the effect that disease could have on the structure and dynamics of plant populations and communities. Harper's book was followed a decade later by Jeremy Burdon's 1987 book Diseases and Plant Population Biology (30). Burdon expanded on the ecological consequences of disease and also emphasized genetic interactions between host and pathogen. Both Harper and Burdon emphasized the relevance of crop research and theories developed in an agricultural context, such as van der Plank's (101) work in epidemiology and Flor's gene-for-gene hypothesis (50). Interestingly, at the same time period, several plant pathologists were discussing disease in natural systems (130). Browning (29), in pa...

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Host-Pathogen Dynamics in Experimental Populations of Silene Alba and Ustilago Violacea. II. Experimental Tests of Theoretical Models

Cited by 77 publications

References 22 publications

Local adaptation in host–parasite systems

Local adaptation in host–parasite systems

LOCAL MALADAPTATION IN THE ANTHER-SMUT FUNGUSMICROBOTRYUM VIOLACEUMTO ITS HOST PLANTSILENE LATIFOLIA: EVIDENCE FROM A CROSS-INOCULATION EXPERIMENT

Disease in Natural Plant Populations, Communities, and Ecosystems: Insights into Ecological and Evolutionary Processes

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