Gilean McVean
University of Oxford
77 Papers
1.2K Citations
Gilean McVean is an academic researcher from University of Oxford. The author has contributed to research in topics: Population & Biology. The author has an hindex of 42, co-authored 77 publications. Previous affiliations of Gilean McVean include University of Cambridge & University of Edinburgh.
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Papers
Growth effects of uniparental disomies and the conflict theory of genomic imprinting
Laurence D. Hurst,Gilean McVean +1 more
TL;DR: The conflict theory proposes that imprinting is an intra-individual manifestation of classical parent-offspring conflict, and is unique in predicting that imprinted genes expressed from the paternally derived genome should be enhancers of pre- and post-natal growth, while those expression from the maternallyderived genome shouldBe growth suppressors.
Estimating recombination rates from population-genetic data
TL;DR: In this article, the authors used population-genetic methods to obtain an accurate measure of how recombination rates vary across the genome, which has implications for understanding the molecular basis of recombination, its evolutionary significance and the distribution of linkage disequilibrium.
The effect of background selection at a single locus on weakly selected, partially linked variants
TL;DR: Both nucleotide site diversity and rates of molecular evolution at a weakly selected locus are affected by background selection as though the effective population size N e is reduced in the same way as for a neutral locus.
Graphical Model Selection for Gaussian Conditional Random Fields in the Presence of Latent Variables.
Abstract: We consider the problem of learning a conditional Gaussian graphical model in the presence of latent variables. Building on recent advances in this field, we suggest a method that decomposes the pa...
Activating mutations in FGFR3 and HRAS reveal a shared genetic origin for congenital disorders and testicular tumors
Anne Goriely,Ruth M. S. Hansen,Indira B. Taylor,Inge A. Olesen,G K Jacobsen,Simon J. McGowan,Susanne P. Pfeifer,Gilean McVean,Ewa Rajpert-De Meyts,Andrew O.M. Wilkie +9 more
TL;DR: It is proposed that paternal age-effect mutations activate a common 'selfish' pathway supporting proliferation in the testis, leading to diverse phenotypes in the next generation including fetal lethality, congenital syndromes and cancer predisposition.