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Alice Mouton

Other affiliations: University of Liège
Bio: Alice Mouton is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Dormouse & Population. The author has an hindex of 8, co-authored 20 publications receiving 133 citations. Previous affiliations of Alice Mouton include University of Liège.

Papers
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Journal ArticleDOI
Giulio Formenti, Kathrin Theissinger, Carlos Fernandes, Iliana Bista, Aureliano Bombarely, Christoph Bleidorn, Claudio Ciofi, Angelica Crottini, José Alberto Godoy Godoy, Jacob Höglund, Joanna Malukiewicz, Alice Mouton, Rebekah A. Oomen, Sadye Paez, Per J. Palsbøll, Christophe Pampoulie, Hannes Svardal, Constantina Theofanopoulou, Jan de Vries, Ann-Marie Waldvogel, Guojie Zhang, Camila J. Mazzoni, Miklós Bálint, Fedor Čiampor, J. Hoglund, María José Ruiz-López, Goujie Zhang, Erich D. Jarvis, Sargis A. Aghayan, Tyler Alioto, Isabel Almudi, Nadir Alvarez, Paulo C. Alves, Isabel R. Amorim, Agostinho Antunes, Paula Arribas, Petr Baldrian, Paul R. Berg, Giorgio Bertorelle, Astrid Böhne, Andrea Bonisoli-Alquati, Ljudevit Luka Boštjančić, Bastien Boussau, Catherine Breton, Elena Buzan, Paula F. Campos, Carlos Carreras, Luis Filipe Castro, Luis J. Chueca, Elena Conti, Robert Cook-Deegan, Daniel Croll, Mónica V. Cunha, Frédéric Delsuc, Alice B. Dennis, Dimitar Dimitrov, Rui Faria, Adrien Favre, Olivier Fedrigo, Rosa Fernández, Gentile Francesco Ficetola, Jean-François Flot, Toni Gabaldón, Dolores R. Galea Agius, Guido Roberto Gallo, Alice Maria Giani, M. Thomas P. Gilbert, Tine Grebenc, Katerina Guschanski, Romain Guyot, Bernhard Hausdorf, Oliver Hawlitschek, Peter D. Heintzman, Berthold Heinze, Michael Hiller, Martin Husemann, Alessio Iannucci, Iker Irisarri, Kjetill S. Jakobsen, Sissel Jentoft, Peter Klinga, Agnieszka Kloch, Claudius F. Kratochwil, Henrik Kusche, Kara K S Layton, Jennifer A. Leonard, Emmanuelle Lerat, Gianni Liti, Tereza Manousaki, Tomas Marques-Bonet, Pável Matos-Maraví, Michael Matschiner, Florian Maumus, Ann M Mc Cartney, Shai Meiri, José Melo-Ferreira, Ximo Mengual, Michael T. Monaghan, Matteo Montagna, Robert W. Mysłajek, Marco T. Neiber, Violaine Nicolas, Marta Novo, Petar Ozretić, Ferran Palero, Lucian Pârvulescu, Marta Pascual, Octávio S. Paulo, Martina Pavlek, Cinta Pegueroles, Loïc Pellissier, Graziano Pesole, Craig R. Primmer, Ana Riesgo, Lukas Rüber, Diego Rubolini, Daniel Salvi, Ole Seehausen, Matthias Seidel, Simona Secomandi, Bruno Studer, Spyros Theodoridis, Marco Thines, Lara Urban, Anti Vasemägi, Adriana Vella, Noel Vella, Sonja C. Vernes, Cristiano Vernesi, David R. Vieites, Robert M. Waterhouse, Christopher W. Wheat, Gert Wörheide, Yannick Wurm, Gabrielle Zammit 
TL;DR: In this article , a large-scale generation of reference genomes representing global biodiversity is discussed. But the authors focus on the large-size generation of the reference genomes and do not discuss how to generate reference genomes for the conservation genomics.
Abstract: Progress in genome sequencing now enables the large-scale generation of reference genomes. Various international initiatives aim to generate reference genomes representing global biodiversity. These genomes provide unique insights into genomic diversity and architecture, thereby enabling comprehensive analyses of population and functional genomics, and are expected to revolutionize conservation genomics.

77 citations

Journal ArticleDOI
04 Mar 2021-Nature
TL;DR: In this article, the authors sequenced five genomes from sub-fossil remains dating from 13,000 to more than 50,000 years ago and found that although they were similar morphologically to the extant grey wolf, dire wolves were a highly divergent lineage that split from living canids around 5.7 million years ago.
Abstract: Dire wolves are considered to be one of the most common and widespread large carnivores in Pleistocene America1, yet relatively little is known about their evolution or extinction. Here, to reconstruct the evolutionary history of dire wolves, we sequenced five genomes from sub-fossil remains dating from 13,000 to more than 50,000 years ago. Our results indicate that although they were similar morphologically to the extant grey wolf, dire wolves were a highly divergent lineage that split from living canids around 5.7 million years ago. In contrast to numerous examples of hybridization across Canidae2,3, there is no evidence for gene flow between dire wolves and either North American grey wolves or coyotes. This suggests that dire wolves evolved in isolation from the Pleistocene ancestors of these species. Our results also support an early New World origin of dire wolves, while the ancestors of grey wolves, coyotes and dholes evolved in Eurasia and colonized North America only relatively recently. Dire wolves split from living canids around 5.7 million years ago and originated in the New World isolated from the ancestors of grey wolves and coyotes, which evolved in Eurasia and colonized North America only relatively recently.

45 citations

Journal ArticleDOI
TL;DR: These findings highlight potential detrimental effects of ARs on a wide variety of species worldwide that may consume poisoned rodents and indicate the need to investigate gene expression effects of other toxicants added to natural environments by humans.
Abstract: Anticoagulant rodenticides (ARs) are indiscriminate toxicants that threaten nontarget predatory and scavenger species through secondary poisoning. Accumulating evidence suggests that AR exposure may have disruptive sublethal consequences on individuals that can affect fitness. We evaluated AR-related effects on genome-wide expression patterns in a population of bobcats in southern California. We identify differential expression of genes involved in xenobiotic metabolism, endoplasmic reticulum stress response, epithelial integrity and both adaptive and innate immune function. Further, we find that differential expression of immune-related genes may be attributable to AR-related effects on leucocyte differentiation. Collectively, our results provide an unprecedented understanding of the sublethal effects of AR exposure on a wild carnivore. These findings highlight potential detrimental effects of ARs on a wide variety of species worldwide that may consume poisoned rodents and indicate the need to investigate gene expression effects of other toxicants added to natural environments by humans.

31 citations

Journal ArticleDOI
TL;DR: This study identifies a functionally distinct subpopulation of TH17 cells with an ability to form TETs containing secreted antimicrobial proteins that capture and kill bacteria.
Abstract: TH17 cell subpopulations have been defined that contribute to inflammation and homeostasis, yet the characteristics of TH17 cells that contribute to host defense against infection are not clear. To elucidate the antimicrobial machinery of the TH17 subset, we studied the response to Cutibacterium acnes, a skin commensal that is resistant to IL-26, the only known TH17-secreted protein with direct antimicrobial activity. We generated C. acnes-specific antimicrobial TH17 clones (AMTH17) with varying antimicrobial activity against C. acnes, which we correlated by RNA sequencing to the expression of transcripts encoding proteins that contribute to antimicrobial activity. Additionally, we validated that AMTH17-mediated killing of C. acnes and bacterial pathogens was dependent on the secretion of granulysin, granzyme B, perforin, and histone H2B. We found that AMTH17 cells can release fibrous structures composed of DNA decorated with histone H2B that entangle C. acnes that we call T cell extracellular traps (TETs). Within acne lesions, H2B and IL-17 colocalized in CD4+ T cells, in proximity to TETs in the extracellular space composed of DNA decorated with H2B. This study identifies a functionally distinct subpopulation of TH17 cells with an ability to form TETs containing secreted antimicrobial proteins that capture and kill bacteria.

30 citations

Journal ArticleDOI
TL;DR: This is the first mitochondrial phylogeography of the common dormouse, Muscardinus avellanarius, a hibernating rodent strictly protected in Europe, and observed low genetic diversity within the sublineages, in contrast to the significant level of genetic differentiation between them.
Abstract: This is the first mitochondrial phylogeography of the common dormouse, Muscardinus avellanarius (Linnaeus, 1758), a hibernating rodent strictly protected in Europe (Habitat Directive, annex IV; Bern Convention, annex III). The 84 individuals of M. avellanarius, sampled throughout the distributional range of the species, have been sequenced at the mitochondrial DNA gene (cytochrome b, 704 base pairs). The results revealed two highly divergent lineages, with an ancient separation around 7.7 Mya and a genetic divergence of 7.7%. Lineage 1 occurs in Western Europe (France, Belgium, and Switzerland) and Italy, and lineage 2 occurs in Central–Northern Europe (Poland, Germany, Latvia, and Lithuania), on the Balkan Peninsula, and in Turkey. Furthermore, these two lineages are subdivided into five sublineages genetically isolated with a strong geographical association. Therefore, lineage 1 branches into two further sublineages (Western European and Italian), whereas lineage 2 contained three sublineages (Central–Northern European, Turkish, and Balkan). We observed low genetic diversity within the sublineages, in contrast to the significant level of genetic differentiation between them. The understanding of genetic population structure is essential for identifying units to be conserved. Therefore, these results may have important implications for M. avellanarius conservation. © 2012 The Linnean Society of London, Biological Journal of the Linnean Society, 2012, 105, 648–664.

24 citations


Cited by
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Journal ArticleDOI
TL;DR: Preface to the Princeton Landmarks in Biology Edition vii Preface xi Symbols used xiii 1.
Abstract: Preface to the Princeton Landmarks in Biology Edition vii Preface xi Symbols Used xiii 1. The Importance of Islands 3 2. Area and Number of Speicies 8 3. Further Explanations of the Area-Diversity Pattern 19 4. The Strategy of Colonization 68 5. Invasibility and the Variable Niche 94 6. Stepping Stones and Biotic Exchange 123 7. Evolutionary Changes Following Colonization 145 8. Prospect 181 Glossary 185 References 193 Index 201

14,171 citations

Journal Article
Fumio Tajima1
30 Oct 1989-Genomics
TL;DR: It is suggested that the natural selection against large insertion/deletion is so weak that a large amount of variation is maintained in a population.

11,521 citations

BookDOI
01 Jan 2011
TL;DR: Firm evidence is provided for Foxp3+CD25+CD4+ Treg cells as an indispensable cellular constituent of the normal immune system for establishing and maintaining immunologic self-tolerance and immune homeostasis.
Abstract: Despite the skepticism that once prevailed among immunologists, it is now widely accepted that the normal immune system harbors a T-cell population, called regulatory T cells (Treg cells), specialized for immune suppression. It was first shown that depletion of a T-cell subpopulation from normal rodents produced autoimmune disease. Search for a molecular marker specific for such autoimmune-preventive Treg cells has revealed that the majority, if not all, of them constitutively express the CD25 molecule as depletion of CD25+CD4+ T cells spontaneously evokes autoimmune disease in otherwise normal rodents. The expression of CD25 by Treg cells has made it possible to delineate their developmental pathways, in particular their thymic development, and establish simple in vitro assay for assessing their suppressive activity. The marker and the in vitro assay have helped to identify human Treg cells with similar functional and phenotypic characteristics. Recent efforts have shown that natural Treg cells specifically express the transcription factor Foxp3 and that mutations of the Foxp3 gene produce a variety of immunological diseases in humans and rodents. Specific expression of Foxp3 in natural Treg cells has enabled their functional and developmental characterization by genetic approach. These studies altogether have provided firm evidence for Foxp3+CD25+CD4+ Treg cells as an indispensable cellular constituent of the normal immune system for establishing and maintaining immunologic self-tolerance and immune homeostasis. Treg cells are now within the scope of clinical use to treat immunological diseases and control physiological and pathological immune responses.

1,745 citations

Journal ArticleDOI
TL;DR: It is shown that whereas spatial approaches are relatively common, spatial replication is generally low and unlikely to provide sufficient environmental variation or power to differentiate competing spatial hypotheses, which highlights the need for large-scale studies that can differentiate competing environmental predictors of immunity.
Abstract: The prevalence and intensity of parasites in wild hosts varies across space and is a key determinant of infection risk in humans, domestic animals and threatened wildlife. Because the immune system serves as the primary barrier to infection, replication and transmission following exposure, we here consider the environmental drivers of immunity. Spatial variation in parasite pressure, abiotic and biotic conditions, and anthropogenic factors can all shape immunity across spatial scales. Identifying the most important spatial drivers of immunity could help pre-empt infectious disease risks, especially in the context of how large-scale factors such as urbanization affect defence by changing environmental conditions. We provide a synthesis of how to apply macroecological approaches to the study of ecoimmunology (i.e. macroimmunology). We first review spatial factors that could generate spatial variation in defence, highlighting the need for large-scale studies that can differentiate competing environmental predictors of immunity and detailing contexts where this approach might be favoured over small-scale experimental studies. We next conduct a systematic review of the literature to assess the frequency of spatial studies and to classify them according to taxa, immune measures, spatial replication and extent, and statistical methods. We review 210 ecoimmunology studies sampling multiple host populations. We show that whereas spatial approaches are relatively common, spatial replication is generally low and unlikely to provide sufficient environmental variation or power to differentiate competing spatial hypotheses. We also highlight statistical biases in macroimmunology, in that few studies characterize and account for spatial dependence statistically, potentially affecting inferences for the relationships between environmental conditions and immune defence. We use these findings to describe tools from geostatistics and spatial modelling that can improve inference about the associations between environmental and immunological variation. In particular, we emphasize exploratory tools that can guide spatial sampling and highlight the need for greater use of mixed-effects models that account for spatial variability while also allowing researchers to account for both individual- and habitat-level covariates. We finally discuss future research priorities for macroimmunology, including focusing on latitudinal gradients, range expansions and urbanization as being especially amenable to large-scale spatial approaches. Methodologically, we highlight critical opportunities posed by assessing spatial variation in host tolerance, using metagenomics to quantify spatial variation in parasite pressure, coupling large-scale field studies with small-scale field experiments and longitudinal approaches, and applying statistical tools from macroecology and meta-analysis to identify generalizable spatial patterns. Such work will facilitate scaling ecoimmunology from individual- to habitat-level insights about the drivers of immune defence and help predict where environmental change may most alter infectious disease risk.

84 citations

Journal ArticleDOI
28 Apr 2022-Cell
TL;DR: In this paper , the authors analyzed aging and nutrition studies in simple organisms, rodents, monkeys, and humans to link longevity to conserved growth and metabolic pathways and outline their role in aging and age-related disease.

81 citations