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Human Molecular Genetics Advance Access originally published online on March 4, 2008
Human Molecular Genetics 2008 17(12):1707-1717; doi:10.1093/hmg/ddn061
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Defective body-weight regulation, motor control and abnormal social interactions in Mecp2 hypomorphic mice

Bredford Kerr1, Matías Alvarez-Saavedra1,{dagger}, Mauricio A. Sáez1,2,{dagger}, Alexandra Saona1,2 and Juan I. Young1,*

1 Centro de Estudios Científicos, Valdivia 5110246, Chile 2 Universidad Austral de Chile, Valdivia 905-9100, Chile

* To whom correspondence should be addressed at: Centro de Estudios Científicos, Av. Arturo Prat 514, Valdivia 5110246, Chile. Tel: +56 63234569; Fax: +56 63234517; Email: jyoung{at}cecs.cl

Received November 19, 2007; Accepted February 27, 2008

MeCP2 is an abundant protein that binds to methylated cytosine residues in DNA and regulates transcription. Mutations in MECP2 cause Rett syndrome, a severe neurological disorder that affects approximately 1:10 000 females. Mice lacking MeCP2 have been generated and constitute important models of Rett syndrome. However, it is yet unclear whether certain physiological events are sensitive to a decrease, rather than a complete lack of MeCP2. Here we report that a Mecp2 floxed allele (Mecp2lox) that was generated to allow conditional mutagenesis behaves as a hypomorph and the corresponding mutant mice exhibit phenotypical alterations including body weight gain, motor abnormalities and altered social behavior. Our data reinforce the view that the central nervous system is extremely sensitive to MeCP2 expression levels and suggest that the 3'-UTR of Mecp2 might contain important elements that contribute to the regulation of its stability or processing.

{dagger} The authors wish it to be known that, in their opinion, the second and third authors should be regarded as equal contributors.


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