ORCID Profile
0000-0003-2238-1978
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In Research Link Australia (RLA), "Research Topics" refer to ANZSRC FOR and SEO codes. These topics are either sourced from ANZSRC FOR and SEO codes listed in researchers' related grants or generated by a large language model (LLM) based on their publications.
Evolutionary biology | Wildlife and Habitat Management | Wildlife and habitat management | Environmental Science and Management | Host-parasite interactions | Biological adaptation | Population, Ecological and Evolutionary Genetics | Biological Adaptation
Control of Pests, Diseases and Exotic Species at Regional or Larger Scales | Expanding Knowledge in the Biological Sciences | Flora, Fauna and Biodiversity at Regional or Larger Scales |
Publisher: MDPI AG
Date: 12-02-2022
DOI: 10.3390/PATHOGENS11020241
Abstract: Although the true prevalence of transmissible cancers is not known, these atypical malignancies are likely rare in the wild. The reasons behind this rarity are only partially understood, but the “Perfect Storm hypothesis” suggests that transmissible cancers are infrequent because a precise confluence of tumor and host traits is required for their emergence. This explanation is plausible as transmissible cancers, like all emerging pathogens, will need specific biotic and abiotic conditions to be able to not only emerge, but to spread to detectable levels. Because those conditions would be rarely met, transmissible cancers would rarely spread, and thus most of the time disappear, even though they would regularly appear. Thus, further research is needed to identify the most important factors that can facilitate or block the emergence of transmissible cancers and influence their evolution. Such investigations are particularly relevant given that human activities are increasingly encroaching into wild areas, altering ecosystems and their processes, which can influence the conditions needed for the emergence and spread of transmissible cell lines.
Publisher: Cambridge University Press (CUP)
Date: 25-07-2006
Publisher: Oxford University Press (OUP)
Date: 2011
Publisher: Wiley
Date: 15-02-2018
Abstract: Similar to parasites, malignant cells exploit the host for energy, resources and protection, thereby impairing host health and fitness. Although cancer is widespread in the animal kingdom, its impact on life history traits and strategies have rarely been documented. Devil facial tumour disease (DFTD), a transmissible cancer, afflicting Tasmanian devils (Sarcophilus harrisii), provides an ideal model system to monitor the impact of cancer on host life-history, and to elucidate the evolutionary arms-race between malignant cells and their hosts. Here we provide an overview of parasite-induced host life history (LH) adaptations, then both phenotypic plasticity of LH responses and changes in allele frequencies that affect LH traits of Tasmanian devils in response to DFTD are discussed. We conclude that akin to parasites, cancer can directly and indirectly affect devil LH traits and trigger host evolutionary responses. Consequently, it is important to consider oncogenic processes as a selective force in wildlife.
Publisher: Wiley
Date: 24-04-2019
DOI: 10.1111/EVA.12790
Publisher: Elsevier BV
Date: 07-2007
Abstract: Theoretical and experimental studies have established the dynamic nature of virulence and that, like all traits, it has evolved. Understanding parasite evolution offers a conceptual framework for erse fields and can contribute greatly to decision-making in disease control. Recently, Grech et al. investigated the effects of host genotype-by-parasite genotype interactions on the expression of virulence in an artificial rodent-malaria system. They found that both parasite and host effects explained most of the variance in the virulence, resistance and transmission potential. These findings are a major contribution to the emerging debate on the pros and cons of a coevolutionary approach of virulence evolution they also hold great potential for more effective control strategies.
Publisher: Elsevier BV
Date: 03-2018
DOI: 10.1016/J.TRECAN.2018.01.002
Abstract: Age is one of the strongest predictors of cancer and risk of death from cancer. Cancer is therefore generally viewed as a senescence-related malady. However, cancer also exists at subclinical levels in humans and other animals, but its earlier effects on the body are poorly known by comparison. We argue here that cancer is a significant but ignored burden on the body and is likely to be a strong selective force from early during the lifetime of an organism. It is time to adopt this novel view of malignant pathologies to improve our understanding of the ways in which oncogenic phenomena influence the ecology and evolution of animals long before their negative impacts become evident and fatal.
Publisher: Cambridge University Press (CUP)
Date: 18-02-2016
DOI: 10.1017/S0031182016000147
Abstract: Despite important differences between infectious diseases and cancers, tumour development (neoplasia) can nonetheless be closely compared to infectious disease because of the similarity of their effects on the body. On this basis, we predict that many of the life-history (LH) responses observed in the context of host–parasite interactions should also be relevant in the context of cancer. Parasites are thought to affect LH traits of their hosts because of strong selective pressures like direct and indirect mortality effects favouring, for ex le, early maturation and reproduction. Cancer can similarly also affect LH traits by imposing direct costs and/or indirectly by triggering plastic adjustments and evolutionary responses. Here, we discuss how and why a LH focus is a potentially productive but under-exploited research direction for cancer research, by focusing our attention on similarities between infectious disease and cancer with respect to their effects on LH traits and their evolution. We raise the possibility that LH adjustments can occur in response to cancer via maternal aternal effects and that these changes can be heritable to (adaptively) modify the LH traits of their offspring. We conclude that LH adjustments can potentially influence the transgenerational persistence of inherited oncogenic mutations in populations.
Publisher: Springer Science and Business Media LLC
Date: 08-03-2018
DOI: 10.1038/S41598-018-20934-9
Abstract: Devil Facial Tumour Disease (DFTD), a highly contagious cancer, has decimated Tasmanian devil ( Sarcophilus harrisii ) numbers in the wild. To ensure its long-term survival, a captive breeding program was implemented but has not been as successful as envisaged at its launch in 2005. We therefore investigated the reproductive success of 65 captive devil pair combinations, of which 35 produced offspring (successful pairs) whereas the remaining 30 pairs, despite being observed mating, produced no offspring (unsuccessful pairs). The devils were screened at six MHC Class I-linked microsatellite loci. Our analyses revealed that younger females had a higher probability of being successful than older females. In the successful pairs we also observed a higher difference in total number of heterozygous loci, i.e. when one devil had a high total number of heterozygous loci, its partner had low numbers. Our results therefore suggest that devil reproductive success is subject to disruptive MHC selection, which to our knowledge has never been recorded in any vertebrate. In order to enhance the success of the captive breeding program the results from the present study show the importance of using young (2-year old) females as well as subjecting the devils to MHC genotyping.
Publisher: Elsevier BV
Date: 08-2015
DOI: 10.1016/J.MEEGID.2015.05.027
Abstract: Understanding parasite strategies for evasion, manipulation or exploitation of hosts is crucial for many fields, from ecology to medical sciences. Generally, research has focused on either the host response to parasitic infection, or the parasite virulence mechanisms. More recently, integrated studies of host-parasite interactions have allowed significant advances in theoretical and applied biology. However, these studies still provide a simplistic view of these as mere two-player interactions. Host and parasite are associated with a myriad of microorganisms that could benefit from the improved fitness of their partner. Illustrations of such complex multi-player interactions have emerged recently from studies performed in various taxa. In this conceptual article, we propose how these associated microorganisms may participate in the phenotypic alterations induced by parasites and hence in host-parasite interactions, from an ecological and evolutionary perspective. Host- and parasite-associated microorganisms may participate in the host-parasite interaction by interacting directly or indirectly with the other partner. As a result, parasites may develop (i) the disruptive strategy in which the parasite alters the host microbiota to its advantage, and (ii) the biological weapon strategy where the parasite-associated microorganism contributes to or modulates the parasite's virulence. Some phenotypic alterations induced by parasite may also arise from conflicts of interests between the host or parasite and its associated microorganism. For each situation, we review the literature and propose new directions for future research. Specifically, investigating the role of host- and parasite-associated microorganisms in host-parasite interactions at the in idual, local and regional level will lead to a holistic understanding of how the co-evolution of the different partners influences how the other ones respond, both ecologically and evolutionary. The conceptual framework we propose here is important and relevant to understand the proximate basis of parasite strategies, to predict their evolutionary dynamics and potentially to prevent therapeutic failures.
Publisher: Wiley
Date: 09-1998
Publisher: Springer Science and Business Media LLC
Date: 04-2006
DOI: 10.1038/440756A
Abstract: As prisoners in their living habitat, parasites should be vulnerable to destruction by the predators of their hosts. But we show here that the parasitic gordian worm Paragordius tricuspidatus is able to escape not only from its insect host after ingestion by a fish or frog but also from the digestive tract of the predator. This remarkable tactic enables the worm to continue its life cycle.
Publisher: Wiley
Date: 20-06-2023
DOI: 10.1111/EVA.13569
Abstract: Infectious diseases are a major threat for bio ersity conservation and can exert strong influence on wildlife population dynamics. Understanding the mechanisms driving infection rates and epidemic outcomes requires empirical data on the evolutionary trajectory of pathogens and host selective processes. Phylodynamics is a robust framework to understand the interaction of pathogen evolutionary processes with epidemiological dynamics, providing a powerful tool to evaluate disease control strategies. Tasmanian devils have been threatened by a fatal transmissible cancer, devil facial tumour disease (DFTD), for more than two decades. Here we employ a phylodynamic approach using tumour mitochondrial genomes to assess the role of tumour genetic ersity in epidemiological and population dynamics in a devil population subject to 12 years of intensive monitoring, since the beginning of the epidemic outbreak. DFTD molecular clock estimates of disease introduction mirrored observed estimates in the field, and DFTD genetic ersity was positively correlated with estimates of devil population size. However, prevalence and force of infection were the lowest when devil population size and tumour genetic ersity was the highest. This could be due to either differential virulence or transmissibility in tumour lineages or the development of host defence strategies against infection. Our results support the view that evolutionary processes and epidemiological trade‐offs can drive host‐pathogen coexistence, even when disease‐induced mortality is extremely high. We highlight the importance of integrating pathogen and population evolutionary interactions to better understand long‐term epidemic dynamics and evaluating disease control strategies.
Publisher: Elsevier BV
Date: 03-2008
Publisher: Public Library of Science (PLoS)
Date: 02-10-2018
Publisher: Wiley
Date: 13-03-2020
DOI: 10.1111/EVA.12938
Abstract: Although transmissible cancers have, so far, only been documented in three independent animal groups, they not only impact animals that have high economic, environmental and social significance, but they are also one of the most virulent parasitic life forms. Currently known transmissible cancers traverse terrestrial and marine environments, and are predicted to be more widely distributed across animal groups thus, the implementation of effective collaborative scientific networks is important for combating existing and emerging forms. Here, we quantify how collaborative effort on the three known transmissible cancers has advanced through the formation of collaborative networks among institutions and disciplines. These three cancers occur in bivalves (invertebrates—disseminated neoplasia DN), Tasmanian devils (vertebrate—marsupial devil facial tumour disease DFTD) and dogs (vertebrate—eutherian mammal canine transmissible venereal tumour CTVT). Research on CTVT and DN has been conducted since 1876 and 1969, respectively, whereas systematic research on DFTD only started in 2006. Yet, collaborative effort on all three diseases is global, encompassing six major Scopus subject areas. Collaborations steadily increased between 1963 and 2006 for CTVT and DN, with similar acceleration for all three cancers since 2006. Network analyses demonstrated that scientists are organizing themselves into efficient collaborative networks however, these networks appear to be far stronger for DFTD and DN, possibly due to the recent detection of new strains adding impetus to research and associated publications (enhancing citation trajectories). In particular, global and multidisciplinary collaborations formed almost immediately after DFTD research was initiated, leading to similar research effort and relatively greater research outputs compared to the other two diseases. Therefore, in the event of outbreaks of new lineages of existing transmissible cancers, or the discovery of new transmissible cancers in the future, the rapid formation of international collaborations spanning relevant disciplines is vital for the efficient management of these diseases.
Publisher: Wiley
Date: 03-2006
Abstract: Proteomics research has developed until recently in a relative isolation from other fast-moving disciplines such as ecology and evolution. This is unfortunate since applying proteomics to these disciplines has apparently the potential to open new perspectives. The huge majority of species indeed exhibit over their entire geographic range a metapopulation structure, occupying habitats that are fragmented and heterogeneous in space and/or through time. Traditionally, population genetics is the main tool used to studying metatopulations, as it describes the spatial structure of populations and the level of gene flow between them. In this Viewpoint, we present the reasons why we think that proteomics, because of the level of integration it promotes, has the potential to resolve interesting issues specific to metapopulation biology and adaptive processes.
Publisher: Oxford University Press (OUP)
Date: 09-03-2005
Publisher: Elsevier BV
Date: 02-2003
Publisher: Elsevier BV
Date: 09-1998
Publisher: Elsevier BV
Date: 04-2018
DOI: 10.1016/J.TREE.2018.01.012
Abstract: Evolved dependence is a process through which one species becomes 'dependent' on another following a long evolutionary history of interaction. This happens when adaptations selected in the first species for interacting lead to fitness costs when the second species is not encountered. Evolved dependence is frequent in host-parasite interactions, where hosts may achieve a higher fitness in the presence of the parasite than in its absence. Since oncogenic manifestations are (i) ubiquitous across multicellular life, (ii) involved in parasitic-like interactions with their hosts, and (iii) have effectively driven the selection of numerous adaptations, it is possible that multicellular organisms display evolved dependence in response to oncogenic processes. We provide a comprehensive overview of the topic, including the implications for cancer prevention and treatment.
Publisher: The Royal Society
Date: 21-03-2018
Abstract: Genetic ersity is essential for adaptive capacities, providing organisms with the potential of successfully responding to intrinsic and extrinsic challenges. Although a clear reciprocal link between genetic ersity and resistance to parasites and pathogens has been established across taxa, the impact of loss of genetic ersity by inbreeding on the emergence and progression of non-communicable diseases, such as cancer, has been overlooked. Here we provide an overview of such associations and show that low genetic ersity and inbreeding associate with an increased risk of cancer in both humans and animals. Cancer being a multifaceted disease, loss of genetic ersity can directly (via accumulation of oncogenic homozygous mutations) and indirectly (via increased susceptibility to oncogenic pathogens) impact abnormal cell emergence and escape of immune surveillance. The observed link between reduced genetic ersity and cancer in wildlife may further imperil the long-term survival of numerous endangered species, highlighting the need to consider the impact of cancer in conservation biology. Finally, the somewhat incongruent data originating from human studies suggest that the association between genetic ersity and cancer development is multifactorial and may be tumour specific. Further studies are therefore crucial in order to elucidate the underpinnings of the interactions between genetic ersity, inbreeding and cancer.
Publisher: The Royal Society
Date: 14-08-2006
Abstract: Phylogenetically unrelated parasites often increase the chances of their transmission by inducing similar phenotypic changes in their hosts. However, it is not known whether these convergent strategies rely on the same biochemical precursors. In this paper, we explored such aspects by studying two gammarid species ( Gammarus insensibilis and Gammarus pulex Crustacea: Amphipoda: Gammaridae) serving as intermediate hosts in the life cycle of two distantly related parasites: the trematode, Microphallus papillorobustus and the acanthocephalan, Polymorphus minutus . Both these parasite species are known to manipulate the behaviour of their hipod hosts, bringing them towards the water surface, where they are preferentially eaten by aquatic birds (definitive hosts). By studying and comparing the brains of infected G. insensibilis and G. pulex with proteomics tools, we have elucidated some of the proximate causes involved in the parasite-induced alterations of host behaviour for each system. Protein identifications suggest that altered physiological compartments in hosts can be similar (e.g. immunoneural connexions) or different (e.g. vision process), and hence specific to the host–parasite association considered. Moreover, proteins required to alter the same physiological compartment can be specific or conversely common in both systems, illustrating in the latter case a molecular convergence in the proximate mechanisms of manipulation.
Publisher: University of Chicago Press
Date: 08-2018
DOI: 10.1086/697963
Abstract: Behavioral ecologists have hypothesized that among-in idual differences in resting metabolic rate (RMR) may predict consistent in idual differences in mean values for costly behaviors or for behaviors that affect energy intake rate. This hypothesis has empirical support and presently attracts considerable attention, but, notably, it does not provide predictions for in idual differences in (a) behavioral plasticity or (b) unexplained variation (residual variation from mean in idual behavior, here termed predictability). We outline how consideration of aerobic maximum metabolic rate (MMR) and particularly aerobic scope (= MMR - RMR) can be used to simultaneously make predictions about mean and among- and within-in idual variation in behavior. We predict that while RMR should be proportional to an in idual's mean level of sustained behavioral activity (one aspect of its personality), in iduals with greater aerobic scope will also have greater scope to express behavioral plasticity and/or greater unpredictability in behavior (=greater residual variation). As a first step toward testing these predictions, we analyze existing activity data from selectively bred lines of mice that differ in both daily activity and aerobic scope. We find that replicate high-scope mice are more active on average and show greater among-in idual variation in activity, greater among-in idual variation in plasticity, and greater unpredictability. These data provide some tentative first support for our hypothesis, suggesting that further research on this topic would be valuable.
Publisher: Wiley
Date: 28-06-2019
DOI: 10.1111/EVA.12831
Publisher: Elsevier BV
Date: 03-2006
DOI: 10.1016/J.BEPROC.2005.10.005
Abstract: Ex les of behavioural manipulation by parasites are numerous, but the processes underlying these changes are not well characterized. From an evolutionary point of view, behavioural changes in infected hosts have often been interpreted as illustrations of the extended phenotype concept, in which genes in one organism (the parasite) have phenotypic effects on another organism (the host). Here, we approach the problem differently, suggesting that hosts, by cooperating with manipulative parasites rather than resisting them, might mitigate fitness costs associated with manipulation. By imposing extra fitness costs on their hosts in the absence of compliance, parasites theoretically have the potential to select for cooperative behaviour by their hosts. Although this 'mafia-like' strategy remains poorly documented, we believe that it has substantial potential to resolve issues specific to the evolution of behavioural alterations induced by parasites.
Publisher: Wiley
Date: 28-02-1970
DOI: 10.1111/EVA.13190
Abstract: The application of evolutionary and ecological principles to cancer prevention and treatment, as well as recognizing cancer as a selection force in nature, has gained impetus over the last 50 years. Following the initial theoretical approaches that combined knowledge from interdisciplinary fields, it became clear that using the eco‐evolutionary framework is of key importance to understand cancer. We are now at a pivotal point where accumulating evidence starts to steer the future directions of the discipline and allows us to underpin the key challenges that remain to be addressed. Here, we aim to assess current advancements in the field and to suggest future directions for research. First, we summarize cancer research areas that, so far, have assimilated ecological and evolutionary principles into their approaches and illustrate their key importance. Then, we assembled 33 experts and identified 84 key questions, organized around nine major themes, to pave the foundations for research to come. We highlight the urgent need for broadening the portfolio of research directions to stimulate novel approaches at the interface of oncology and ecological and evolutionary sciences. We conclude that progressive and efficient cross‐disciplinary collaborations that draw on the expertise of the fields of ecology, evolution and cancer are essential in order to efficiently address current and future questions about cancer.
Publisher: Cambridge University Press (CUP)
Date: 11-12-2019
DOI: 10.1017/S0031182019001501
Abstract: Although there is a plethora of cancer associated-factors that can ultimately culminate in death (cachexia, organ impairment, metastases, opportunistic infections, etc.), the focal element of every terminal malignancy is the failure of our natural defences to control unlimited cell proliferation. The reasons why our defences apparently lack efficiency is a complex question, potentially indicating that, under Darwinian terms, solutions other than preventing cancer progression are also important contributors. In analogy with host-parasite systems, we propose to call this latter option ‘tolerance’ to cancer. Here, we argue that the ubiquity of oncogenic processes among metazoans is at least partially attributable to both the limitations of resistance mechanisms and to the evolution of tolerance to cancer. Deciphering the ecological contexts of alternative responses to the cancer burden is not a semantic question, but rather a focal point in understanding the evolutionary ecology of host-tumour relationships, the evolution of our defences, as well as why and when certain cancers are likely to be detrimental for survival.
Publisher: Wiley
Date: 18-10-2022
DOI: 10.1111/MEC.16721
Abstract: A plethora of intrinsic and environmental factors have been shown to influence the length of telomeres, the protector of chromosome ends. Despite the growing interest in infection–telomere interactions, there is very limited knowledge on how transmissible cancers influence telomere maintenance. An emblematic ex le of transmissible cancer occurs in the Tasmanian devil ( Sarcophilus harrisii ), whose populations have been dramatically reduced by infectious cancer cells. To investigate associations between telomere dynamics and the transmissible cancer, we used longitudinal data from a Tasmanian devil population that has been exposed to the disease for over 15 years. We detected substantial temporal variation in in idual telomere length (TL), and a positive significant association between TL and age, as well as a marginally significant trend for devils with devil facial tumour disease (DFTD) having longer telomeres. A proportional hazard analysis yielded no significant effect of TL on the development of DFTD. Like previous studies, we show the complexity that TL dynamics may exhibit across the lifetime of organisms. Our work highlights the importance of long‐term longitudinal s ling for understanding the effects of wildlife diseases on TL.
Publisher: The Royal Society
Date: 31-08-2005
Abstract: The parasitic Nematomorph hairworm, Spinochordodes tellinii (Camerano) develops inside the terrestrial grasshopper, Meconema thalassinum (De Geer) (Orthoptera: Tettigoniidae), changing the insect's responses to water. The resulting aberrant behaviour makes infected insects more likely to jump into an aquatic environment where the adult parasite reproduces. We used proteomics tools (i.e. two-dimensional gel electrophoresis (2-DE), computer assisted comparative analysis of host and parasite protein spots and MALDI-TOF mass spectrometry) to identify these proteins and to explore the mechanisms underlying this subtle behavioural modification. We characterized simultaneously the host (brain) and the parasite proteomes at three stages of the manipulative process, i.e. before, during and after manipulation. For the host, there was a differential proteomic expression in relation to different effects such as the circadian cycle, the parasitic status, the manipulative period itself, and worm emergence. For the parasite, a differential proteomics expression allowed characterization of the parasitic and the free-living stages, the manipulative period and the emergence of the worm from the host. The findings suggest that the adult worm alters the normal functions of the grasshopper's central nervous system (CNS) by producing certain ‘effective’ molecules. In addition, in the brain of manipulated insects, there was found to be a differential expression of proteins specifically linked to neurotransmitter activities. The evidence obtained also suggested that the parasite produces molecules from the family Wnt acting directly on the development of the CNS. These proteins show important similarities with those known in other insects, suggesting a case of molecular mimicry. Finally, we found many proteins in the host's CNS as well as in the parasite for which the function(s) are still unknown in the published literature (www) protein databases. These results support the hypothesis that host behavioural changes are mediated by a mix of direct and indirect chemical manipulation.
Publisher: Wiley
Date: 29-01-2020
DOI: 10.1111/EVA.12920
Abstract: Strong and ongoing artificial selection in domestic animals has resulted in amazing phenotypic responses that benefit humans, but often at a cost to an animal's health, and problems related to inbreeding depression, including a higher incidence of cancer. Despite high rates of cancer in domesticated species, little attention has been devoted to exploring the hypothesis that persistent artificial selection may also favour the evolution of compensatory anticancer defences. Indeed, there is evidence for effective anti‐cancer defences found in several domesticated species associated with different cancer types. We also suggest that artificial selection can favour the “domestication” of inherited oncogenic mutations in rare instances, retaining those associated to late and/or less aggressive cancers, and that by studying these seemingly rare anticancer adaptations, novel cancer treatments may be found.
Publisher: Wiley
Date: 15-03-2022
DOI: 10.1111/MEC.16408
Abstract: Understanding the effects of wildlife diseases on populations requires insight into local environmental conditions, host defence mechanisms, host life‐history trade‐offs, pathogen population dynamics, and their interactions. The survival of Tasmanian devils ( Sarcophilus harrisii ) is challenged by a novel, fitness limiting pathogen, Tasmanian devil facial tumour disease (DFTD), a clonally transmissible, contagious cancer. In order to understand the devils’ capacity to respond to DFTD, it is crucial to gain information on factors influencing the devils’ immune system. By using RT‐qPCR, we investigated how DFTD infection in association with intrinsic (sex and age) and environmental (season) factors influences the expression of 10 immune genes in Tasmanian devil blood. Our study showed that the expression of immune genes (both innate and adaptive) differed across seasons, a pattern that was altered when infected with DFTD. The expression of immunogbulins IgE and IgM:IgG showed downregulation in colder months in DFTD infected animals. We also observed strong positive association between the expression of an innate immune gene, CD16, and DFTD infection. Our results demonstrate that s ling across seasons, age groups and environmental conditions are beneficial when deciphering the complex ecoevolutionary interactions of not only conventional host‐parasite systems, but also of host and diseases with high mortality rates, such as transmissible cancers.
Publisher: Wiley
Date: 02-08-2006
DOI: 10.1111/J.1365-2583.2006.00671.X
Abstract: Despite increasing evidence of host phenotypic manipulation by parasites, the underlying mechanisms causing infected hosts to act in ways that benefit the parasite remain enigmatic in most cases. Here, we used proteomics tools to identify the biochemical alterations that occur in the head of the cricket Nemobius sylvestris when it is driven to water by the hairworm Paragordius tricuspidatus. We characterized host and parasite proteomes during the expression of the water-seeking behaviour. We found that the parasite produces molecules from the Wnt family that may act directly on the development of the central nervous system (CNS). In the head of manipulated cricket, we found differential expression of proteins specifically linked to neurogenesis, circadian rhythm and neurotransmitter activities. We also detected proteins for which the function(s) are still unknown. This proteomics study on the biochemical pathways altered by hairworms has also allowed us to tackle questions of physiological and molecular convergence in the mechanism(s) causing the alteration of orthoptera behaviour. The two hairworm species produce effective molecules acting directly on the CNS of their orthoptera hosts.
Publisher: Elsevier BV
Date: 11-2008
Publisher: Oxford University Press (OUP)
Date: 2009
Publisher: Wiley
Date: 23-03-2020
DOI: 10.1111/EVA.12948
Abstract: Ecological and evolutionary concepts have been widely adopted to understand host–pathogen dynamics, and more recently, integrated into wildlife disease management. Cancer is a ubiquitous disease that affects most metazoan species however, the role of oncogenic phenomena in eco‐evolutionary processes and its implications for wildlife management and conservation remains undeveloped. Despite the pervasive nature of cancer across taxa, our ability to detect its occurrence, progression and prevalence in wildlife populations is constrained due to logistic and diagnostic limitations, which suggests that most cancers in the wild are unreported and understudied. Nevertheless, an increasing number of virus‐associated and directly transmissible cancers in terrestrial and aquatic environments have been detected. Furthermore, anthropogenic activities and sudden environmental changes are increasingly associated with cancer incidence in wildlife. This highlights the need to upscale surveillance efforts, collection of critical data and developing novel approaches for studying the emergence and evolution of cancers in the wild. Here, we discuss the relevance of malignant cells as important agents of selection and offer a holistic framework to understand the interplay of ecological, epidemiological and evolutionary dynamics of cancer in wildlife. We use a directly transmissible cancer (devil facial tumour disease) as a model system to reveal the potential evolutionary dynamics and broader ecological effects of cancer epidemics in wildlife. We provide further ex les of tumour–host interactions and trade‐offs that may lead to changes in life histories, and epidemiological and population dynamics. Within this framework, we explore immunological strategies at the in idual level as well as transgenerational adaptations at the population level. Then, we highlight the need to integrate multiple disciplines to undertake comparative cancer research at the human–domestic–wildlife interface and their environments. Finally, we suggest strategies for screening cancer incidence in wildlife and discuss how to integrate ecological and evolutionary concepts in the management of current and future cancer epizootics.
Publisher: Wiley
Date: 26-12-2016
DOI: 10.1111/EVA.12444
Publisher: Elsevier
Date: 2017
Publisher: Wiley
Date: 11-2019
DOI: 10.1111/EVA.12862
Publisher: Public Library of Science (PLoS)
Date: 06-06-2019
No related organisations have been discovered for Frederic THOMAS.
Start Date: 2023
End Date: 12-2025
Amount: $387,788.00
Funder: Australian Research Council
View Funded ActivityStart Date: 04-2019
End Date: 12-2023
Amount: $300,000.00
Funder: Australian Research Council
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