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The Journal of Neuroscience, December 31, 2008, 28(53):14341-14346; doi:10.1523/JNEUROSCI.2390-08.2008

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Brief Communications
The Bifunctional microRNA miR-9/miR-9* Regulates REST and CoREST and Is Downregulated in Huntington's Disease

Amy N. Packer,^1,5 Yi Xing,^1,4 Scott Q. Harper,⁶ Lesley Jones,^7,8 and Beverly L. Davidson^1,2,3,5

Departments of ¹Internal Medicine, ²Molecular Physiology & Biophysics, ³Neurology, and ⁴Biomedical Engineering and ⁵Program in Molecular and Cellular Biology, University of Iowa, Iowa City, Iowa 52242, ⁶Department of Pediatrics, The Ohio State University, Columbus, Ohio 43205, and ⁷Department of Psychological Medicine and ⁸Institute of Medical Genetics, Wales School of Medicine, Cardiff University, Cardiff CF14 4XN, United Kingdom

Correspondence should be addressed to Beverly L. Davidson, University of Iowa, Department of Internal Medicine, Room 200, Eckstein Medical Research Building, Iowa City, IA 52242. Email: beverly-davidson{at}uiowa.edu

The transcription factor REST silences neuronal gene expression in non-neuronal cells. In neurons, the protein is sequestered in the cytoplasm in part through binding to huntingtin. Polyglutamine expansions in huntingtin, which causes Huntington's disease (HD), abrogates REST-huntingtin binding. Consequently, REST translocates to the nucleus, occupies RE1 repressor sequences and decreases neuronal gene expression. In this work, we found that levels of several microRNAs (miRNAs) with upstream RE1 sites are decreased in HD patient cortices relative to healthy controls. Interestingly, one of these, the bifunctional brain enriched miR-9/miR-9*, targets two components of the REST complex: miR-9 targets REST and miR-9* targets CoREST. These data provide evidence for a double negative feedback loop between the REST silencing complex and the miRNAs it regulates.

Key words: miRNA; REST; Huntington's disease; cortex; coordination; RNA interference

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Received May 27, 2008; revised Nov. 10, 2008; accepted Nov. 13, 2008.

Correspondence should be addressed to Beverly L. Davidson, University of Iowa, Department of Internal Medicine, Room 200, Eckstein Medical Research Building, Iowa City, IA 52242. Email: beverly-davidson{at}uiowa.edu

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