Journal
PLOS ONE
Volume 8, Issue 1, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0051436
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Funding
- National Institutes of Health (NIH) [MH080434, MH07897, P30HD03352, T32 GM07215]
- International Rett Syndrome Foundation (IRSF)
- Postbaccalaureate Research and Education Program fellowships (PREP) [NIH/R25 GM075149]
- Minority Access to Research Careers fellowship (MARC) [NIH/T34 GM008510]
- University of Wisconsin-Madison Center for Stem Cells and Regenerative Medicine
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Background: Epigenetic mechanisms, including DNA methylation, histone modification, and microRNAs, play pivotal roles in stem cell biology. Methyl-CpG binding protein 1 (MBD1), an important epigenetic regulator of adult neurogenesis, controls the proliferation and differentiation of adult neural stem/progenitor cells (aNSCs). We recently demonstrated that MBD1 deficiency in aNSCs leads to altered expression of several noncoding microRNAs (miRNAs). Methodology/Principal Findings: Here we show that one of these miRNAs, miR-195, and MBD1 form a negative feedback loop. While MBD1 directly represses the expression of miR-195 in aNSCs, high levels of miR-195 in turn repress the expression of MBD1. Both gain-of-function and loss-of-function investigations show that alterations of the MBD1-miR-195 feedback loop tip the balance between aNSC proliferation and differentiation. Conclusions/Significance: Therefore the regulatory loop formed by MBD1 and miR-195 is an important component of the epigenetic network that controls aNSC fate.
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