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Human Molecular Genetics Advance Access published online on March 4, 2008
Human Molecular Genetics, 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, Mauricio A. Sáez1,2, Alexandra Saona1,2 and Juan I. Young1,*

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

* Corresponding author: Juan I. Young. Av. Arturo Prat 514 Valdivia, Chile. 5110246. Tel: +56 63 234569; Fax: +56 63 234517; Email: jyoung{at}cecs.cl

Received November 19, 2007; Revised February 27, 2008; 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 3UTR of Mecp2 might contain important elements that contribute to the regulation of its stability or processing.

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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