Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

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Record number 421409
Title Serial translocation by means of circular intermediates underlies colour sidedness in cattle
Author(s) Durkin, K.; Coppieters, W.; Drogemuller, C.; Ahariz, N.; Cambisano, N.; Druet, T.; Fasquelle, C.; Haile, A.; Horin, P.; Huang, L.; Kamatani, Y.; Karim, L.; Lathrop, M.; Moser, S.; Oldenbroek, J.K.; Rieder, S.; Sartelet, A.; Sölkner, J.; Stalhammer, H.; Zelenika, D.; Zhang, Z.; Leeb, T.; Georges, M.; Charlier, C.
Source Nature 482 (2012). - ISSN 0028-0836 - p. 81 - 84.
Department(s) Centrum voor Genetische Bronnen Nederland
Publication type Refereed Article in a scientific journal
Publication year 2012
Keyword(s) copy number - gene - expression - pattern - genome
Abstract Colour sidedness is a dominantly inherited phenotype of cattle characterized by the polarization of pigmented sectors on the flanks, snout and ear tips1. It is also referred to as ‘lineback’ or ‘witrik’ (which means white back), as colour-sided animals typically display a white band along their spine. Colour sidedness is documented at least since the Middle Ages and is presently segregating in several cattle breeds around the globe, including in Belgian blue and brown Swiss1, 2. Here we report that colour sidedness is determined by a first allele on chromosome 29 (Cs29), which results from the translocation of a 492-kilobase chromosome 6 segment encompassing KIT to chromosome 29, and a second allele on chromosome 6 (Cs6), derived from the first by repatriation of fused 575-kilobase chromosome 6 and 29 sequences to the KIT locus. We provide evidence that both translocation events involved circular intermediates. This is the first example, to our knowledge, of a phenotype determined by homologous yet non-syntenic alleles that result from a novel copy-number-variant-generating mechanism
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