TY - JOUR A1 - Schwensow, Nina A1 - Mazzoni, Camila J. A1 - Marmesat, Elena A1 - Fickel, Jörns A1 - Peacock, David A1 - Kovaliski, John A1 - Sinclair, Ron A1 - Cassey, Phillip A1 - Cooke, Brian A1 - Sommer, Simone T1 - High adaptive variability and virus-driven selection on major histocompatibility complex (MHC) genes in invasive wild rabbits in Australia JF - Biological invasions : unique international journal uniting scientists in the broad field of biological invasions N2 - The rabbit haemorrhagic disease virus (RHDV) was imported into Australia in 1995 as a biocontrol agent to manage one of the most successful and devastating invasive species, the European rabbit (Oryctolagus cuniculus cuniculus). During the first disease outbreaks, RHDV caused mortality rates of up to 97% and reduced Australian rabbit numbers to very low levels. However, recently increased genetic resistance to RHDV and strong population growth has been reported. Major histocompatibility complex (MHC) class I immune genes are important for immune responses against viruses, and a high MHC variability is thought to be crucial in adaptive processes under pathogen-driven selection. We asked whether strong population bottlenecks and presumed genetic drift would have led to low MHC variability in wild Australian rabbits, and if the retained MHC variability was enough to explain the increased resistance against RHD. Despite the past bottlenecks we found a relatively high number of MHC class I sequences distributed over 2-4 loci. We identified positive selection on putative antigen-binding sites of the MHC. We detected evidence for RHDV-driven selection as one MHC supertype was negatively associated with RHD survival, fitting expectations of frequency-dependent selection. Gene duplication and pathogen-driven selection are possible (and likely) mechanisms that maintained the adaptive potential of MHC genes in Australian rabbits. Our findings not only contribute to a better understanding of the evolution of invasive species, they are also important in the light of planned future rabbit biocontrol in Australia. KW - Major histocompatibility complex (MHC) KW - Australian rabbit invasion KW - Rabbit haemorrhagic disease virus (RHDV) KW - Virus-driven selection KW - Adaptive genetic variability Y1 - 2017 U6 - https://doi.org/10.1007/s10530-016-1329-5 SN - 1387-3547 SN - 1573-1464 VL - 19 SP - 1255 EP - 1271 PB - Springer CY - Dordrecht ER - TY - JOUR A1 - Schuster, Andrea C. A1 - Herde, Antje A1 - Mazzoni, Camila J. A1 - Eccard, Jana A1 - Sommer, Simone T1 - Evidence for selection maintaining MHC diversity in a rodent species despite strong density fluctuations JF - Immunogenetics N2 - Strong spatiotemporal variation in population size often leads to reduced genetic diversity limiting the adaptive potential of individual populations. Key genes of adaptive variation are encoded by the immune genes of the major histocompatibility complex (MHC) playing an essential role in parasite resistance. How MHC variation persists in rodent populations that regularly experience population bottlenecks remains an important topic in evolutionary genetics. We analysed the consequences of strong population fluctuations on MHC class II DRB exon 2 diversity in two distant common vole (Microtus arvalis) populations in three consecutive years using a high-throughput sequencing approach. In 143 individuals, we detected 25 nucleotide alleles translating into 14 unique amino acid MHC alleles belonging to at least three loci. Thus, the overall allelic diversity and amino acid distance among the remaining MHC alleles, used as a surrogate for the range of pathogenic antigens that can be presented to T-cells, are still remarkably high. Both study populations did not show significant population differentiation between years, but significant differences were found between sites. We concluded that selection processes seem to be strong enough to maintain moderate levels of MHC diversity in our study populations outcompeting genetic drift, as the same MHC alleles were conserved between years. Differences in allele frequencies between populations might be the outcome of different local parasite pressures and/or genetic drift. Further understanding of how pathogens vary across space and time will be crucial to further elucidate the mechanisms maintaining MHC diversity in cyclic populations. KW - MHC diversity KW - Selection KW - High-throughput next-generation sequencing KW - Population cycle KW - Common vole KW - Microtus arvalis Y1 - 2016 U6 - https://doi.org/10.1007/s00251-016-0916-z SN - 0093-7711 SN - 1432-1211 VL - 68 SP - 429 EP - 437 PB - Springer CY - New York ER - TY - GEN A1 - Hartmann, Stefanie A1 - Hasenkamp, Natascha A1 - Mayer, Jens A1 - Michaux, Johan A1 - Morand, Serge A1 - Mazzoni, Camila J. A1 - Roca, Alfred L. A1 - Greenwood, Alex D. T1 - Endogenous murine leukemia retroviral variation across wild European and inbred strains of house mouse T2 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe N2 - Background: Endogenous murine leukemia retroviruses (MLVs) are high copy number proviral elements difficult to comprehensively characterize using standard low throughput sequencing approaches. However, high throughput approaches generate data that is challenging to process, interpret and present. Results: Next generation sequencing (NGS) data was generated for MLVs from two wild caught Mus musculus domesticus (from mainland France and Corsica) and for inbred laboratory mouse strains C3H, LP/J and SJL. Sequence reads were grouped using a novel sequence clustering approach as applied to retroviral sequences. A Markov cluster algorithm was employed, and the sequence reads were queried for matches to specific xenotropic (Xmv), polytropic (Pmv) and modified polytropic (Mpmv) viral reference sequences. Conclusions: Various MLV subtypes were more widespread than expected among the mice, which may be due to the higher coverage of NGS, or to the presence of similar sequence across many different proviral loci. The results did not correlate with variation in the major MLV receptor Xpr1, which can restrict exogenous MLVs, suggesting that endogenous MLV distribution may reflect gene flow more than past resistance to infection. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1329 KW - murine leukemia virus KW - endogenous retrovirus KW - Xpr1 KW - XMRV KW - genomic evolution KW - Markov cluster algorithm Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-431200 SN - 1866-8372 IS - 1329 ER - TY - JOUR A1 - Hartmann, Stefanie A1 - Hasenkamp, Natascha A1 - Mayer, Jens A1 - Michaux, Johan A1 - Morand, Serge A1 - Mazzoni, Camila J. A1 - Roca, Alfred L. A1 - Greenwood, Alex D. T1 - Endogenous murine leukemia retroviral variation across wild European and inbred strains of house mouse JF - BMC genomics N2 - Background: Endogenous murine leukemia retroviruses (MLVs) are high copy number proviral elements difficult to comprehensively characterize using standard low throughput sequencing approaches. However, high throughput approaches generate data that is challenging to process, interpret and present. Results: Next generation sequencing (NGS) data was generated for MLVs from two wild caught Mus musculus domesticus (from mainland France and Corsica) and for inbred laboratory mouse strains C3H, LP/J and SJL. Sequence reads were grouped using a novel sequence clustering approach as applied to retroviral sequences. A Markov cluster algorithm was employed, and the sequence reads were queried for matches to specific xenotropic (Xmv), polytropic (Pmv) and modified polytropic (Mpmv) viral reference sequences. Conclusions: Various MLV subtypes were more widespread than expected among the mice, which may be due to the higher coverage of NGS, or to the presence of similar sequence across many different proviral loci. The results did not correlate with variation in the major MLV receptor Xpr1, which can restrict exogenous MLVs, suggesting that endogenous MLV distribution may reflect gene flow more than past resistance to infection. KW - Murine leukemia virus KW - Endogenous retrovirus KW - Xpr1 KW - XMRV KW - Genomic evolution KW - Markov cluster algorithm Y1 - 2015 U6 - https://doi.org/10.1186/s12864-015-1766-z SN - 1471-2164 VL - 16 PB - BioMed Central CY - London ER -