L1 retrotransposition in neurons is modulated by MeCP2
Alysson R. Muotri (),
Maria C. N. Marchetto,
Nicole G. Coufal,
Ruth Oefner,
Gene Yeo,
Kinichi Nakashima and
Fred H. Gage ()
Additional contact information
Alysson R. Muotri: University of California San Diego, School of Medicine, Stem Cell Program
Maria C. N. Marchetto: Laboratory of Genetics, The Salk Institute for Biological Studies
Nicole G. Coufal: Laboratory of Genetics, The Salk Institute for Biological Studies
Ruth Oefner: Laboratory of Genetics, The Salk Institute for Biological Studies
Gene Yeo: University of California San Diego, School of Medicine, Stem Cell Program, 9500 Gilman Dr, La Jolla, California 92093-0695, USA
Kinichi Nakashima: Laboratory of Molecular Neuroscience, Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan
Fred H. Gage: Laboratory of Genetics, The Salk Institute for Biological Studies
Nature, 2010, vol. 468, issue 7322, 443-446
Abstract:
Retrotransposition in neurons L1 retrotransposons are dynamically regulated and active genomic elements that affect gene expression and neuronal function throughout brain development. According to a new study by Alysson Muotri and colleagues, the absence of MeCP2, a modulator of DNA methylation implicated in several neurodevelopmental disorders, increases L1 retrotransposon activity in rodent models. This increase in susceptibility to L1 retrotransposition is duplicated in iPS cells derived from patients with Rett syndrome. These data correlations suggest that disease-related genetic mutations may influence L1 retrotransposon activity, adding another layer of complexity to our understanding of molecular neurological disorders.
Date: 2010
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DOI: 10.1038/nature09544
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