Research Group 2: Evolutionary Genetics
Research Group 2: Evolutionary Genetics |
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Fragmentation of habitat can have severe impacts on the dynamics and demography of populations by limiting suitable habitat, migration and gene exchange among populations. As a consequence, populations in small fragments become isolated and the negative effects of inbreeding or genetic drift may increase. In this part of our project we investigate the relative importance of forest cover and functional connectivity of forest fragments for the population dynamics of small mammal species. Small mammal species respond in different ways to the fragmentation of the forest habitat. Habitat generalists are - in contrast to specialist species - not impaired by fragmentation of the forest habitat. We concentrate mainly on specialist rodent and marsupial species sensitive to forest fragmentation. In three landscapes with different amount of forest cover (15 %, 31 %, and 43 %) and one control area of continuous forest we study demographic population parameters by using capture-mark-recapture methods. The number of marked individuals and the recapture data of individuals after different time intervals are used to run population models in order to estimate survival-, reproduction-, and immigration rates of the small mammal populations. These estimates provide the possibility to understand source-sink-dynamics of the different populations within a landscape as well as – in comparison between landscapes – the impact of the amount of remaining forest on the demography of small mammal populations. |
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Limitations to migration and the occurrence of genetic drift and inbreeding due to habitat fragmentation may have a severe impact on the genetic diversity of populations. In the mammalian immune system the genes of the MHC play a key role in parasite and pathogen resistance. It is claimed that a lack of variation at the MHC may increase the susceptibility to infectious diseases which might pose severe problems to small populations and especially to the persistence of endangered species. Parasites and pathogens are able to control a host population in size, rate of growth and demography. However, there are also examples of species ‘doing well’ with low MHC diversity. It remains unclear why some species or even different populations of the same species differ in their ability to cope with these challenges. How much MHC diversity is required to ensure long-term population viability remains a fundamental question in conservation genetics. In this project, we investigate the importance of overall genetic variability and adaptive MHC-diversity in parasite resistance as well as the genetic and fitness consequences of fragmentation in small mammal species inhabiting the Brazilian Mata Atlântica with different levels of genetic diversity. The selected species (Akodon montensis, Delomys sublineatus, Oryzomys russatus, O. angouya, Gracilinanus microtarsus, Marmosops incanus) differ in their sensitivity to anthropogenic influences. Some species only occur in larger parts of rainforest whereas others can cope with a fragmented landscape.
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The genes of the major histocompatibility complex (MHC) are one side in a co-evolutionary arms race between host and parasites. MHC genes encode cell surface glycoproteins of the hosts responsible for antigen recognition. Their variability is directly linked with parasite resistance and individual fitness. Understanding the effects of immune gene constitution on pathogens resistance is one of the most important questions in the conservation of endangered species. Allelic polymorphism is, however, not the only source of variability subjected to natural selection. Genetic variation may also exist in gene expression patterns and might explain why species differ in their ability to adapt to changing environmental and parasitological conditions. In this study, we investigate how expression levels of certain MHC genes differ with respect to parasitic infections by using real-time PCR. Elucidating the role of MHC gene expression in an evolutionary ecological context could provide the functional basis to improve our understanding why some species react more sensitive to fragmentation than others which is currently one of the ‘hottest’ issues in conservation genetics. We focus on three different species:
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Under natural conditions, pathogens are strong selective forces that drive coevolutionary processes. Studies on selective mechanisms in host species largely concentrated on analyses of host major histocompatibility complex (MHC) sequence variation but did not take the variance in the expression levels of MHC and other immunologically relevant genes into account. However, this variance might be of evolutionary importance, in particular in response to fast evolving viruses. But how viruses remodel the host’s gene expression patterns and the genetic constitution of host populations is still elusive.
In this project, we investigate the importance of the variability on the structural and transcriptional level of immunologically relevant genes in relation to a severe contagious viral infection, the rabbit haemorrhagic disease (RHD) raging in European rabbits (Oryctolagus cuniculus). Outbreaks result in the deaths of a high number of free-living and domestic rabbits whereas some rabbits survive the outbreaks. The comparison between RHD-susceptible and resistant rabbits by using a microarray approach combined with qRT-PCR of selected genes allows us to test current selection hypotheses in more detail. The identification of multiple regulatory mechanisms will improve our understanding of causes and processes of evolutionary adaptations between hosts and pathogens.
This project is part of the DFG Priority Program ‘Host-Parasite Coevolution – Rapid reciprocal adaptation and its genetic basis’ funded by the German Science Foundation (SPP 1399, DFG SO 428/7-1).
Principal investigator: Prof. Dr. Simone Sommer
in collaboration
with Dr. Jörns Fickel (IZW, Berlin) and Dr. Brian Cooke (University
of Canberra, Australia)
Postdoc: Dr. Nina Schwensow
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During the last few decades increasing desertification processes through expanding land use have had severe degradation and fragmentation effects on southern Africa’s environments. Anthropogenic impact coupled to climate change pose a severe threat to the survival of many mammalian taxa currently occupying the region by negatively influencing community structure, population ecology and the genetic variability. In particular small mammals play an important role in ecosystems and numerous species are highly vulnerable due to their restricted dispersal capabilities. Habitat fragmentation has a substantial impact upon the distribution of species and consequently genetic lineages and diversity. Genetic diversity is associated with fitness parameters such as the immune competence of populations which buffers them against widespread pathogens and parasites. Both habitat degradation and climatic conditions are also crucial parameters in terms of distribution, transmission and developmental success of both parasites and pathogens. Such changes may have significant implications for outbreak patterns of pest host species, the conservation of rare host mammal species and their ecological functions, as well as associated veterinary and medical consequences for wildlife, lifestock and humans. We study the effects of different land use on parasite burden and immune gene variability (MHC) of small mammals along a precipitation gradient through South Africa and Namibia to investigate the importance of the MHC-constitution for resistance to gastrointestinal parasites. Further, the analysis of hostspecific variations of the endoparasite diversity and genetic adaptations of host organisms along a climatic gradient might provide insights into coevolutionary processes and could contribute to a deeper understanding of the consequences of global warming. The results of the study should be conducive to the comprehension of functional biodiversity changes resulting from desertification as well as the genetic basis of evolutionary ecology. |
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Scientific goals are expression analyses of immune genes (MHC) as well as investigations of the effects of diverse extrinsic factors on the immune system of large African carnivores.
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Mate choice is one of the most important evolutionary
mechanisms. A growing number of studies indicate that
females can increase the viability of their offspring
by gaining direct benefits such as parental care or
by gaining genetic advantages through selective mating
with certain males. Genetic benefits can be obtained
if the risk of genetic incompatibility between maternal
and paternal genomes is minimised by avoiding mating
with close kin (inbreeding avoidance), or by increasing
the genetic heterozygosity or diversity within the progeny.
Among the best candidates for the genetic basis of mate
choice in vertebrates are the genes of the major histocompatibility
complex (MHC). The MHC plays an important role in the
vertebrate immune system and also provides direct olfactory
cues for mate choice. According to current hypotheses
females might choose males with different MHC-alleles
as mating partners to increase the genetic variability
of offspring and thus their resistance to infectious
diseases. Free living primates are interesting models
to investigate MHC-associated mate choice due to the
wide variance of different social organisations and
mating systems which potentially allow the detection
of universal mechanisms of adaptive evolution. In cooperation with Dr. K Dausmann, Univ. Hamburg; Dr. M Eberle, Deutsches Primatenzentrum Göttingen; Dr. J Fietz, Univ. Ulm. Supported by the German Science Foundation (DFG So 428/4-1 and 428/4-2). |
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Main
research projects and goals: Evolutionary Genetics (RG 2)
