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- Ameen, Carly, et al.
(författare)
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Specialized sledge dogs accompanied Inuit dispersal across the North American Arctic
- 2019
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Ingår i: Proceedings of the Royal Society of London. Biological Sciences. - : The Royal Society. - 0962-8452 .- 1471-2954. ; 286:1916
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Tidskriftsartikel (refereegranskat)abstract
- Domestic dogs have been central to life in the North American Arctic for millennia. The ancestors of the Inuit were the first to introduce the widespread usage of dog sledge transportation technology to the Americas, but whether the Inuit adopted local Palaeo-Inuit dogs or introduced a new dog population to the region remains unknown. To test these hypotheses, we generated mitochondrial DNA and geometric morphometric data of skull and dental elements from a total of 922 North American Arctic dogs and wolves spanning over 4500 years. Our analyses revealed that dogs from Inuit sites dating from 2000 BP possess morphological and genetic signatures that distinguish them from earlier Palaeo-Inuit dogs, and identified a novel mitochondrial clade in eastern Siberia and Alaska. The genetic legacy of these Inuit dogs survives today in modern Arctic sledge dogs despite phenotypic differences between archaeological and modern Arctic dogs. Together, our data reveal that Inuit dogs derive from a secondary pre-contact migration of dogs distinct from Palaeo-Inuit dogs, and probably aided the Inuit expansion across the North American Arctic beginning around 1000 BP.
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- Harris, Alison J. T., 1982-, et al.
(författare)
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Diversity in Labrador Inuit sled dog diets : Insights from δ13C and δ15N analysis of dog bone and dentine collagen
- 2020
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Ingår i: Journal of Archaeological Science. - : Elsevier BV. - 2352-409X .- 2352-4103. ; 32
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Tidskriftsartikel (refereegranskat)abstract
- Sled dogs were an integral part of Labrador Inuit life from the initial expansion and settlement of northeastern Canada to the present day. Tasked with pulling sleds and assisting people with other subsistence activities in the winter, dogs required regular provisioning with protein and fat. In this paper, we conduct stable carbon and nitrogen isotope ratio analysis of the skeletal remains of dogs (n=35) and wild fauna (n=68) from sites located on the north and south coasts of Labrador to characterize dog provisioning between the 15th to early 19th centuries. In addition, we analyse bone (n=20) and dentine (n=4) collagen from dogs from Double Mer Point, a communal house site in Hamilton Inlet to investigate how dog diets intersected with Inuit subsistence and trade activities at a local level. We find that dog diets were largely composed of marine mammal protein, but that dogs on the north coast consumed more caribou and fish relative to dogs from the central and south coast sites. The diets of dogs from Double Mer Point were the most heterogenous of any site, suggesting long-distance movement of people and/or animals along the coast.
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- Nmezi, Bruce, et al.
(författare)
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An oligodendrocyte silencer element underlies the pathogenic impact of lamin B1 structural variants
- 2023
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Ingår i: bioRxiv : the preprint server for biology. - : Cold Spring Harbor Laboratory Press (CSHL).
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Tidskriftsartikel (refereegranskat)abstract
- The role of non-coding regulatory elements and how they might contribute to tissue type specificity of disease phenotypes is poorly understood. Autosomal Dominant Leukodystrophy (ADLD) is a fatal, adult-onset, neurological disorder that is characterized by extensive CNS demyelination. Most cases of ADLD are caused by tandem genomic duplications involving the lamin B1 gene ( LMNB1 ) while a small subset are caused by genomic deletions upstream of the gene. Utilizing data from recently identified families that carry LMNB1 gene duplications but do not exhibit demyelination, ADLD patient tissues, CRISPR modified cell lines and mouse models, we have identified a novel silencer element that is lost in ADLD patients and that specifically targets overexpression to oligodendrocytes. This element consists of CTCF binding sites that mediate three-dimensional chromatin looping involving the LMNB1 and the recruitment of the PRC2 repressor complex. Loss of the silencer element in ADLD identifies a previously unknown role for silencer elements in tissue specificity and disease causation.
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