House mouse colonization patterns on the sub-Antarctic Kerguelen Archipelago suggest singular primary invasions and resilience against re-invasion.

BACKGROUND: Starting from Western Europe, the house mouse (Mus musculus domesticus) has spread across the globe in historic times. However, most oceanic islands were colonized by mice only within the past 300 years. This makes them an excellent model for studying the evolutionary processes during early stages of new colonization. We have focused here on the Kerguelen Archipelago, located within the sub-Antarctic area and compare the patterns with samples from other Southern Ocean islands. RESULTS: We have typed 18 autosomal and six Y-chromosomal microsatellite loci and obtained mitochondrial D-loop sequences for a total of 534 samples, mainly from the Kerguelen Archipelago, but also from the Falkland Islands, Marion Island, Amsterdam Island, Antipodes Island, Macquarie Island, Auckland Islands and one sample from South Georgia. We find that most of the mice on the Kerguelen Archipelago have the same mitochondrial haplotype and all share the same major Y-chromosomal haplotype. Two small islands (Cochons Island and Cimetière Island) within the archipelago show a different mitochondrial haplotype, are genetically distinct for autosomal loci, but share the major Y-chromosomal haplotype. In the mitochondrial D-loop sequences, we find several single step mutational derivatives of one of the major mitochondrial haplotypes, suggesting an unusually high mutation rate, or the occurrence of selective sweeps in mitochondria. CONCLUSIONS: Although there was heavy ship traffic for over a hundred years to the Kerguelen Archipelago, it appears that the mice that have arrived first have colonized the main island (Grande Terre) and most of the associated small islands. The second invasion that we see in our data has occurred on islands that are detached from Grande Terre and were likely to have had no resident mice prior to their arrival. The genetic data suggest that the mice of both primary invasions originated from related source populations. Our data suggest that an area colonized by mice is refractory to further introgression, possibly due to fast adaptations of the resident mice to local conditions.

Copy number changes of CNV regions in intersubspecific crosses of the house mouse.

Copy number variation (CNV) contributes significantly to natural genetic variation within and between populations. However, the mutational mechanisms leading to CNV, as well as the processes that control the size of CNV regions, are so far not well understood. Here, we have analyzed a gene family that forms CNV regions on the X and the Y chromosomes in Mus musculus. These CNV regions show copy number differences in two subspecies, M. musculus domesticus and M. musculus musculus. Assessment of copy numbers at these loci for individuals caught in a natural hybrid zone showed copy number increases and a large variance among individuals. Crosses of natural hybrid animals among each other produced even more extreme variants with major differences in copy number in the offspring from the same parents. To assess the inheritance pattern of the loci further, we have produced F1 and backcross hybrid animals from these subspecies. We found that copy number expansions can already be traced in F1 offspring and they became stronger in the backcross individuals. Specific analysis of hybrid male offspring indicated that neither meiotic recombination nor interchromosomal exchange was required for creating these changes because the X and Y chromosomes have no homologues in males. This suggests that intrachromosomal exchanges can drive CNV and that this can occur at an elevated frequency in interspecific crosses, even within an individual. Accordingly, we find copy number mosaicism in individuals, that is, DNA from different tissues of the same individual can have different copy numbers for the loci studied. A preliminary survey of autosomal loci suggests that these can also be subject to change in hybrids. Hence, we conclude that the effects we see are not only restricted to some specific loci but may also be caused by a general induction of replication-coupled repair processes.

The Drosophila melanogaster T-box genes midline and H15 are conserved regulators of heart development.

The Drosophila melanogaster genes midline and H15 encode predicted T-box transcription factors homologous to vertebrate Tbx20 genes. All identified vertebrate Tbx20 genes are expressed in the embryonic heart and we find that both midline and H15 are expressed in the cardioblasts of the dorsal vessel, the insect organ equivalent to the vertebrate heart. The midline mRNA is first detected in dorsal mesoderm at embryonic stage 12 in the two progenitors per hemisegment that will divide to give rise to all six cardioblasts. Expression of H15 mRNA in the dorsal mesoderm is detected first in four to six cells per hemisegment at stage 13. The expression of midline and H15 in the dorsal vessel is dependent on Wingless signaling and the transcription factors tinman and pannier. We find that the selection of two midline-expressing cells from a pool of competent progenitors is dependent on Notch signaling. Embryos deleted for both midline and H15 have defects in the alignment of the cardioblasts and associated pericardial cells. Embryos null for midline have weaker and less penetrant phenotypes while embryos deficient for H15 have morphologically normal hearts, suggesting that the two genes are partially redundant in heart development. Despite the dorsal vessel defects, embryos mutant for both midline and H15 have normal numbers of cardioblasts, suggesting that cardiac cell fate specification is not disrupted. However, ectopic expression of midline in the dorsal mesoderm can lead to dramatic increases in the expression of cardiac markers, suggesting that midline and H15 participate in cardiac fate specification and may normally act redundantly with other cardiogenic factors. Conservation of Tbx20 expression and function in cardiac development lends further support for a common ancestral origin of the insect dorsal vessel and the vertebrate heart.