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PLP Summary: L1 retrotransposition in neurons is modulated by MeCP2
Muotri et al. 2010. Nature 468: 443-6.
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Rett syndrome, a neurodevelopment disorder, could be caused by an increase in susceptibility to L1
retrotransposition, a new study suggests.
Alysson Muotri of the University of California San Diego and her colleagues showed that MeCP2, a
protein involved in global DNA methylation, acts to repress long interspersed nuclear element-1 (LINE-1
or L1) expression in neural stem cells and mouse neuroepithelial cells. The authors also found that brain
tissue of Rett patients displays an increase in L1 retrotransposition. To measure retrotransposotion,
Muotri developed a new technique based on single-cell quantitative PCR (qPCR) that could quantify the
number of new L1 insertions in the genome of a single cell. The mutation in MeCP2 carried by Rett
patients appears to cause increased L1 expression and retrotransposition in brain tissue, which could
impact the genome and interfere with normal gene expression. However, other actions of MeCP2 are not
known, leaving open the possibility that MeCP2 acts as an inhibiter or activator of other genes as well.
The symptoms of Rett syndrome could be caused by the inability of mutant MeCP2 to affect these other
genes, and not by increased L1 retrotransposition.