Native to China and Mongolia, the brown rat (Rattus norvegicus) now enjoys a worldwide distribution. While black rats and the house mouse tracked the regional development of human agricultural settlements, brown rats did not appear in Europe until the 1500s, suggesting their range expansion was a response to relatively recent increases in global trade. We inferred the global phylogeography of brown rats using 32 k SNPs, and detected 13 evolutionary clusters within five expansion routes. One cluster arose following a southward expansion into Southeast Asia. Three additional clusters arose from two independent eastward expansions: one expansion from Russia to the Aleutian Archipelago, and a second to western North America. Westward expansion resulted in the colonization of Europe from which subsequent rapid colonization of Africa, the Americas and Australasia occurred, and multiple evolutionary clusters were detected. An astonishing degree of fine-grained clustering between and within sampling sites underscored the extent to which urban heterogeneity shaped genetic structure of commensal rodents. Surprisingly, few individuals were recent migrants, suggesting that recruitment into established populations is limited. Understanding the global population structure of R. norvegicus offers novel perspectives on the forces driving the spread of zoonotic disease, and aids in development of rat eradication programmes.

Once restricted to northern China and Mongolia, the brown rat (Rattus norvegicus) now enjoys a worldwide distribution due to the evolution of commensalism with humans. In contrast to black rats and the house mouse, which have tracked the regional and global development of human agricultural settlements, brown rats do not appear in the European historical record until the 1500s, suggesting their range expansion was a response to relatively recent increases in global trade and modern sea-faring. We inferred the global phylogeography of brown rats using 32k SNPs to reconstruct invasion routes from estimates of population divergence and admixture. Globally, we detected 13 evolutionary clusters within five expansion routes. One cluster arose following a southward expansion into Southeast Asia. Three additional clusters arose from two independent eastward expansions: one expansion from Russia to the Aleutian Archipelago, and a second to western North America. Rapid westward expansion resulted in the colonization of Europe from which subsequent colonization of Africa, the Americas, and Australasia occurred, and multiple evolutionary clusters were detected. An astonishing degree of fine-grained clustering found both between and within our sampling sites underscored the extent to which urban heterogeneity can shape the genetic structure of commensal rodents. Surprisingly, few individuals were recent migrants despite continual global transport, suggesting that recruitment into established populations is limited. Understanding the global population structure of R. norvegicus offers novel perspectives on the forces driving the spread of zoonotic disease, and yields greater capacity to develop targeted rat eradication programs.

House mouse tissue samples from 30 populations in Germany, Switzerland and the Azores were analyzed for sequence changes in the gene VKORC1, which potentially confer resistance to anticoagulant rodenticides. Except for one population originating from south Germany, sequence variants were found in individuals from all locations analyzed (29 out of 30 sites surveyed), with less than 10 % of the individuals matching the wild-type genotype. The most frequent and widespread amino acid substitutions were Leu128Ser, Tyr139Cys and a group of linked sequence changes (Arg12Trp/Ala26Ser/Ala48Thr/Arg61Leu). These three genotypes occurred either alone or in combination with each other or with other less frequent sequence changes. Where they occurred as the sole variant, the proportion of homozygous animals was 72-83 %, suggesting a high selection pressure due to permanent pest control in these populations.An evaluation of published data revealed that the three frequent sequence changes found are associated with a substantial loss of rodenticide efficacy of first generation anticoagulants (e.g. warfarin, coumatetralyl) as well as the second generation compound bromadiolone and most probably also difenacoum. Further studies are required to investigate the effect on compounds of higher potency, in particular, where combinations of sequence changes occur in one individual.

No abstract

No abstract