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Nucleic Acids Research Advance Access originally published online on February 22, 2008
Nucleic Acids Research 2008 36(7):2320-2329; doi:10.1093/nar/gkn085
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Nucleic Acids Research, 2008, Vol. 36, No. 7 2320-2329
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Position effect variegation and imprinting of transgenes in lymphocytes

Adam Williams, Nicola Harker, Eleni Ktistaki, Henrique Veiga-Fernandes, Kathleen Roderick, Mauro Tolaini, Trisha Norton, Keith Williams and Dimitris Kioussis*

Division of Molecular Immunology, The National Institute for Medical Research, London, NW71AA, UK

*To whom correspondence should be addressed. Tel: +44 20 8816 2194; Fax: +44 20 8816 2248; Email: dkiouss{at}nimr.mrc.ac.uk

Received November 13, 2007. Revised February 11, 2008. Accepted February 11, 2008.

Sequences proximal to transgene integration sites are able to deregulate transgene expression resulting in complex position effect phenotypes. In addition, transgenes integrated as repeated arrays are susceptible to repeat-induced gene silencing. Using a Cre recombinase-based system we have addressed the influence of transgene copy number (CN) on expression of hCD2 transgenes. CN reduction resulted in a decrease, increase or no effect on variegation depending upon the site of integration. This finding argues that repeat-induced gene silencing is not the principle cause of hCD2 transgene variegation. These results also suggest that having more transgene copies can be beneficial at some integration sites. The transgenic lines examined in this report also exhibited a form of imprinting, which was manifested by decreased levels of expression and increased levels of variegation, upon maternal transmission; and this correlated with DNA hypermethylation and a reduction in epigenetic chromatin modifications normally associated with active genes.


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