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No evidence of non‐homologous insertions in mouse model of MDD created by replacement of homologous mouse DNA sequence with pathogenic 6‐base human CREB1 promoter sequence

No evidence of non‐homologous insertions in mouse model of MDD created by replacement of... We have recently reported the creation and initial characterization of the first etiology‐based recombinant mouse model of major depressive disorder (MDD). This was achieved by replacing the corresponding mouse DNA sequence with a 6‐base DNA sequence from the human CREB1 promoter that is associated with the development of MDD in families identified by probands with recurrent, early‐onset MDD. The current study explored whether the desired homologous recombination event at the mouse Creb1 gene that resulted in the creation of the mouse model was also accompanied by insertions of the targeting vector at unintended non‐homologous locations in the mouse genome. No evidence of insertions of targeting vector sequence was observed at regions other than the mouse Creb1 gene. © 2011 Wiley Periodicals, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Medical Genetics Wiley

No evidence of non‐homologous insertions in mouse model of MDD created by replacement of homologous mouse DNA sequence with pathogenic 6‐base human CREB1 promoter sequence

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References (8)

Publisher
Wiley
Copyright
Copyright © 2012 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1552-4841
eISSN
1552-485X
DOI
10.1002/ajmg.b.32006
pmid
22180334
Publisher site
See Article on Publisher Site

Abstract

We have recently reported the creation and initial characterization of the first etiology‐based recombinant mouse model of major depressive disorder (MDD). This was achieved by replacing the corresponding mouse DNA sequence with a 6‐base DNA sequence from the human CREB1 promoter that is associated with the development of MDD in families identified by probands with recurrent, early‐onset MDD. The current study explored whether the desired homologous recombination event at the mouse Creb1 gene that resulted in the creation of the mouse model was also accompanied by insertions of the targeting vector at unintended non‐homologous locations in the mouse genome. No evidence of insertions of targeting vector sequence was observed at regions other than the mouse Creb1 gene. © 2011 Wiley Periodicals, Inc.

Journal

American Journal of Medical Genetics – Wiley

Published: Jan 1, 2012

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