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.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 397792
Title Including copy number variation in association studies to predict genotypic values
Author(s) Calus, M.P.L.; Koning, de, D.J.; Haley, C.S.
Source Genetics Research 92 (2010)2. - ISSN 0016-6723 - p. 115 - 125.
DOI https://doi.org/10.1017/S0016672310000091
Department(s) Research
Publication type Refereed Article in a scientific journal
Publication year 2010
Keyword(s) wide linkage disequilibrium - human genome - mutation-rates - genetic risk - disease - polymorphism - markers - cattle - snps - microsatellite
Abstract The objective of this study was to investigate, both empirically and deterministically, the ability to explain genetic variation resulting from a copy number polymorphism (CNP) by including the CNP, either by its genotype or by a continuous derivation thereof, alone or together with a nearby single nucleotide polymorphism (SNP) in the model. This continuous measure of a CNP genotype could be a raw hybridization measurement, or a predicted CNP genotype. Results from simulations showed that the linkage disequilibrium (LD) between an SNP and CNP was lower than LD between two SNPs, due to the higher mutation rate at the CNP loci. The model R2 values from analysing the simulated data were very similar to the R2 values predicted with the deterministic formulae. Under the assumption that x copies at a CNP locus lead to the effect of x times the effect of 1 copy, including a continuous measure of a CNP locus in the model together with the genotype of a nearby SNP increased power to explain variation at the CNP locus, even when the continuous measure explained only 15% of the variation at the CNP locus.
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