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  • 1
    In: Molecular Ecology, Wiley, Vol. 20, No. 14 ( 2011-07), p. 2929-2941
    Type of Medium: Online Resource
    ISSN: 0962-1083
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2011
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2019
    In:  Journal of Animal Ecology Vol. 88, No. 3 ( 2019-03), p. 427-438
    In: Journal of Animal Ecology, Wiley, Vol. 88, No. 3 ( 2019-03), p. 427-438
    Abstract: Parasite spillover from invasive aliens to native species increases the risk of disease emergence within native biota—either by direct harm to the new host or by indirect effects like increased risks of secondary infection. One example for such a detrimental effect is the parasitic copepod Mytilicola intestinalis that infected blue mussels Mytilus edulis after being introduced into the North Sea in the early 20th century. Since 1949, the parasite was blamed for multiple mass mortalities of infested blue mussels but evidence for a direct causal involvement of M. intestinalis remained circumstantial. Here, we now examine the potential effects of primary infections by the invasive parasite on the susceptibility to secondary infections with virulent bacteria ( Vibrio spp.) in a full factorial infection experiment combining parasite infection (control vs. infected) with different Vibrio infection treatments (control, bath challenge, injection) in environmental conditions that either favoured the host (ambient temperature) or the bacterium (elevated temperature). The influence of primary and secondary infections on cellular immunity (phagocytosis) and Vibrio load in the haemolymph was used to correlate these results to host survival. Our results suggest that the rate of secondary Vibrio infection is increased due to lower efficiency of the cellular immune response. As a consequence, the failure of clearing Vibrio from the haemolymph might increase mortality of mussels infected by M. intestinalis . This demonstrates that indirect effects of parasite invasions can outweigh direct effects of the infection highlighting the need for a more integrative approach to understand and predict the consequences of parasite invasions.
    Type of Medium: Online Resource
    ISSN: 0021-8790 , 1365-2656
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2019
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  • 3
    In: Molecular Ecology, Wiley, Vol. 27, No. 6 ( 2018-03), p. 1505-1519
    Abstract: On theoretical grounds, antagonistic co‐evolution between hosts and their parasites should be a widespread phenomenon but only received little empirical support so far. Consequently, the underlying molecular mechanisms and evolutionary steps remain elusive, especially in nonmodel systems. Here, we utilized the natural history of invasive parasites to document the molecular underpinnings of co‐evolutionary trajectories. We applied a dual‐species transcriptomics approach to experimental cross‐infections of blue mussel Mytilus edulis hosts and their invasive parasitic copepods Mytilicola intestinalis from two invasion fronts in the Wadden Sea. We identified differentially regulated genes from an experimental infection contrast for hosts (infected vs. control) and a sympatry contrast (sympatric vs. allopatric combinations) for both hosts and parasites. The damage incurred by Mytilicola infection and the following immune response of the host were mainly reflected in cell division processes, wound healing, apoptosis and the production of reactive oxygen species ( ROS ). Furthermore, the functional coupling of host and parasite sympatry contrasts revealed the concerted regulation of chitin digestion by a Chitotriosidase 1 homolog in hosts with several cuticle proteins in the parasite. Together with the coupled regulation of ROS producers and antagonists, these genes represent candidates that mediate the different evolutionary trajectories within the parasite's invasion. The host–parasite combination‐specific coupling of these effector mechanisms suggests that underlying recognition mechanisms create specificity and local adaptation. In this way, our study demonstrates the use of invasive species’ natural history to elucidate molecular mechanisms of host–parasite co‐evolution in the wild.
    Type of Medium: Online Resource
    ISSN: 0962-1083 , 1365-294X
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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    detail.hit.zdb_id: 1126687-9
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  • 4
    In: Global Change Biology, Wiley, Vol. 28, No. 1 ( 2022-01), p. 54-71
    Abstract: Rapid climate change is placing many marine species at risk of local extinction. Recent studies show that epigenetic mechanisms (e.g. DNA methylation, histone modifications) can facilitate both within and transgenerational plasticity to cope with changing environments. However, epigenetic reprogramming (erasure and re‐establishment of epigenetic marks) during gamete and early embryo development may hinder transgenerational epigenetic inheritance. Most of our knowledge about reprogramming stems from mammals and model organisms, whereas the prevalence and extent of reprogramming among non‐model species from wild populations is rarely investigated. Moreover, whether reprogramming dynamics are sensitive to changing environmental conditions is not well known, representing a key knowledge gap in the pursuit to identify mechanisms underlying links between parental exposure to changing climate patterns and environmentally adapted offspring phenotypes. Here, we investigated epigenetic reprogramming (DNA methylation/hydroxymethylation) and gene expression across gametogenesis and embryogenesis of marine stickleback ( Gasterosteus aculeatus ) under three ocean warming scenarios (ambient, +1.5 and +4°C). We found that parental acclimation to ocean warming led to dynamic and temperature‐sensitive reprogramming throughout offspring development. Both global methylation/hydroxymethylation and expression of genes involved in epigenetic modifications were strongly and differentially affected by the increased warming scenarios. Comparing transcriptomic profiles from gonads, mature gametes and early embryonic stages showed sex‐specific accumulation and temperature sensitivity of several epigenetic actors. DNA methyltransferase induction was primarily maternally inherited (suggesting maternal control of remethylation), whereas induction of several histone‐modifying enzymes was shaped by both parents. Importantly, massive, temperature‐specific changes to the epigenetic landscape occurred in blastula, a critical stage for successful embryo development, which could, thus, translate to substantial consequences for offspring phenotype resilience in warming environments. In summary, our study identified key stages during gamete and embryo development with temperature‐sensitive reprogramming and epigenetic gene regulation, reflecting potential ‘windows of opportunity’ for adaptive epigenetic responses under future climate change.
    Type of Medium: Online Resource
    ISSN: 1354-1013 , 1365-2486
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2020313-5
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  • 5
    In: Functional Ecology, Wiley, Vol. 28, No. 6 ( 2014-12), p. 1482-1493
    Abstract: Our study addresses the role of non‐genetic and genetic inheritance in shaping the adaptive potential of populations under a warming ocean scenario. We used a combined experimental approach [transgenerational plasticity ( TGP ) and quantitative genetics] to partition the relative contribution of maternal vs. paternal (additive genetic) effects to offspring body size (a key component of fitness), and investigated a potential physiological mechanism (mitochondrial respiration capacities) underlying whole‐organism growth/size responses. In very early stages of growth (up to 30 days), offspring body size of marine sticklebacks benefited from maternal TGP : offspring of mothers acclimated to 17 °C were larger when reared at 17 °C, and offspring of mothers acclimated to 21 °C were larger when reared at 21 °C. The benefits of maternal TGP on body size were stronger and persisted longer (up to 60 days) for offspring reared in the warmer (21 °C) environment, suggesting that maternal effects will be highly relevant for climate change scenarios in this system. Mitochondrial respiration capacities measured on mature offspring (F1 adults) matched the pattern of TGP for juvenile body size, providing an intuitive mechanistic basis for the maternal acclimation persisting into adulthood. Size differences between temperatures seen at early growth stages remained in the F1 adults, linking offspring body size to maternal inheritance of mitochondria. Lower maternal variance components in the warmer environment were mostly driven by mothers acclimated to ambient (colder) conditions, further supporting our tenet that maternal effects were stronger at elevated temperature. Importantly, all parent–offspring temperature combination groups showed genotype × environment (G × E) interactions, suggesting that reaction norms have the potential to evolve. To summarize, TGP and G × E interactions work in concert to mediate impacts of ocean warming on metabolic capacity and early growth of marine sticklebacks. TGP can buffer short‐term detrimental effects of climate warming and may buy time for genetic adaptation to catch up, therefore markedly contributing to the evolutionary potential and persistence of populations under climate change.
    Type of Medium: Online Resource
    ISSN: 0269-8463 , 1365-2435
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2014
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    detail.hit.zdb_id: 619313-4
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  • 6
    In: Molecular Ecology, Wiley, Vol. 21, No. 4 ( 2012-02), p. 779-781
    Type of Medium: Online Resource
    ISSN: 0962-1083
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2020749-9
    detail.hit.zdb_id: 1126687-9
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  • 7
    In: Environmental Microbiology, Wiley, Vol. 25, No. 8 ( 2023-08), p. 1424-1438
    Abstract: Phages depend on their bacterial hosts to replicate. The habitat, density and genetic diversity of host populations are therefore key factors in phage ecology, but our ability to explore their biology depends on the isolation of a diverse and representative collection of phages from different sources. Here, we compared two populations of marine bacterial hosts and their phages collected during a time series sampling program in an oyster farm. The population of Vibrio crassostreae , a species associated specifically to oysters, was genetically structured into clades of near clonal strains, leading to the isolation of closely related phages forming large modules in phage–bacterial infection networks. For Vibrio chagasii , which blooms in the water column, a lower number of closely related hosts and a higher diversity of isolated phages resulted in small modules in the phage–bacterial infection network. Over time, phage load was correlated with V. chagasii abundance, indicating a role of host blooms in driving phage abundance. Genetic experiments further demonstrated that these phage blooms can generate epigenetic and genetic variability that can counteract host defence systems. These results highlight the importance of considering both the environmental dynamics and the genetic structure of the host when interpreting phage–bacteria networks.
    Type of Medium: Online Resource
    ISSN: 1462-2912 , 1462-2920
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2020213-1
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  • 8
    In: Journal of Animal Ecology, Wiley, Vol. 92, No. 5 ( 2023-05), p. 991-1000
    Abstract: Predators can affect parasite–host interactions when directly preying on hosts or their parasites. However, predators may also have non‐consumptive indirect effects on parasite–host interactions when hosts adjust their behaviour or physiology in response to predator presence. In this study, we examined how chemical cues from a predatory marine crab affect the transmission of a parasitic trematode from its first (periwinkle) to its second (mussel) intermediate host. Laboratory experiments revealed that chemical cues from crabs lead to a threefold increase in the release of trematode cercariae from periwinkles as a result of increased periwinkle activity. This positive effect on transmission was contrasted by a 10‐fold reduction in cercarial infection rates in the second intermediate host when we experimentally exposed mussels to cercariae and predator cues. The low infection rates were caused by a substantial reduction in mussel filtration activity in the presence of predator cues, preventing cercariae from entering the mussels. To assess the combined net effect of both processes, we conducted a transmission experiment between infected periwinkles and uninfected mussels. Infection levels of mussels in the treatments with crab cues were sevenfold lower than in mussels without crab chemical cues. This suggests that predation risk effects on mussel susceptibility can counteract the elevated parasite release from first intermediate hosts, with negative net effects on parasite transmission. These experiments highlight that predation risk effects on parasite transmission can have opposing directions at different stages of the parasite's life cycle. Such complex non‐consumptive predation risk effects on parasite transmission may constitute an important indirect mechanism affecting prevalence and distribution patterns of parasites in different hosts across their life cycle.
    Type of Medium: Online Resource
    ISSN: 0021-8790 , 1365-2656
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2006616-8
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  • 9
    Online Resource
    Online Resource
    Wiley ; 2008
    In:  Evolution Vol. 62, No. 9 ( 2008-09), p. 2381-2392
    In: Evolution, Wiley, Vol. 62, No. 9 ( 2008-09), p. 2381-2392
    Type of Medium: Online Resource
    ISSN: 0014-3820 , 1558-5646
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 2036375-8
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  • 10
    In: Evolutionary Applications, Wiley, Vol. 10, No. 4 ( 2017-04), p. 338-347
    Abstract: The consequences of emerging marine diseases on the evolutionary trajectories of affected host populations in the marine realm are largely unexplored. Evolution in response to natural selection depends on the genetic variation of the traits under selection and the interaction of these traits with the environment (GxE). However, in the case of diseases, pathogen genotypes add another dimension to this interaction. Therefore, the study of disease resistance needs to be extended to the interaction of host genotype, pathogen genotype and environment (GxGxE). In this study, we used a full‐sib breeding design crossing two genetically differentiated populations of the Pacific oyster Crassostrea gigas (Thunberg, 1793), to determine the influence of host genotype, pathogen genotype and temperature on disease resistance. Based on a controlled infection experiment on two early life stages, that is, D‐larvae and Pediveliger larvae at elevated and ambient water temperatures, we estimated disease resistance to allopatric and sympatric Vibrio sp . by measuring survival and growth within and between genetically differentiated oyster populations. In both populations, survival was higher upon infection with sympatric Vibrio sp ., indicating that disease resistance has a genetic basis and is dependent on host genotype. In addition, we observed a significant GxGxE effect in D‐larvae, where contrary to expectations, disease resistance was higher at warm than at cold temperatures. Using thermal reaction norms, we could further show that disease resistance is an environment dependent trait with high plasticity, which indicates the potential for a fast acclimatization to changing environmental conditions. These population‐specific reaction norms disappeared in hybrid crosses between both populations which demonstrates that admixture between genetically differentiated populations can influence GxGxE interactions on larger scales.
    Type of Medium: Online Resource
    ISSN: 1752-4571 , 1752-4571
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2405496-3
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