4 results match your criteria: "1 Max Planck Institute for Evolutionary Biology[Affiliation]"
Biol Lett
December 2018
1 Max Planck Institute for Evolutionary Biology, August-Thienemann-Strasse 2, 24306 Plön , Germany.
During mate choice decisions, females of many vertebrates use male olfactory cues to achieve immunogenetic optimality of their offspring. Three-spined sticklebacks ( Gasterosteus aculeatus) populating habitats that differ in their parasite communities evolve locally adapted combinations of genetic variants encoded at the major histocompatibility complex (MHC). Such adaptation confers optimal resistance to the local parasite fauna.
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March 2015
1] Max Planck Institute for Evolutionary Biology, August-Thienemann-Strasse 2, D-24306 Plön, Germany [2] Institute for Experimental Medicine, Christian-Albrechts-University of Kiel, Arnold-Heller-Strasse 3, D-24105 Kiel, Germany.
Recent evidence suggests that natural selection operating on hosts to maintain their microbiome contributes to the emergence of new species, that is, the 'hologenomic basis of speciation'. Here we analyse the gut microbiota of two house mice subspecies, Mus musculus musculus and M. m.
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January 2015
1] Department of Ecology, Evolution and Behavior, University of Minnesota, St Paul, Minnesota 55108, USA [2] The BioTechnology Institute, University of Minnesota, St Paul, Minnesota 55108, USA.
Complex life has arisen through a series of 'major transitions' in which collectives of formerly autonomous individuals evolve into a single, integrated organism. A key step in this process is the origin of higher-level evolvability, but little is known about how higher-level entities originate and gain the capacity to evolve as an individual. Here we report a single mutation that not only creates a new level of biological organization, but also potentiates higher-level evolvability.
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April 2014
1] Max Planck Institute for Evolutionary Biology, August-Thienemann-Street 2, D-24306 Plön, Germany [2] Department of Dermatology, University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany.
Susceptibility to chronic inflammatory diseases is determined by immunogenetic and environmental risk factors. Resident microbial communities often differ between healthy and diseased states, but whether these differences are of primary aetiological importance or secondary to the altered inflammatory environment remains largely unknown. Here we provide evidence for host gene-microbiota interactions contributing to disease risk in a mouse model of epidermolysis bullosa acquisita, an autoantibody-induced inflammatory skin disease.
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