期刊
STEM CELLS
卷 28, 期 6, 页码 1060-1070出版社
WILEY
DOI: 10.1002/stem.431
关键词
miR-137; MicroRNA; Neural stem cells; Adult neurogenesis; Dendritic development; Neuronal maturation
资金
- International Rett Syndrome Foundation (IRSF)
- NIH [NS051630, MH076090, MH080434, MH078972]
- Beckman Young Investigator Award
- Basil O'Connor Scholar Research Award
- Alfred P. Sloan Research Fellow in Neuroscience
- Autism Speaks Postdoctoral Fellowship
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R25GM060201] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R56MH076090, R01MH076090, R01MH078972, R01MH080434] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS051630] Funding Source: NIH RePORTER
The maturation of young neurons is regulated by complex mechanisms and dysregulation of this process is frequently found in neurodevepmental disorders. MicroRNAs have been implicated in several steps of neuronal maturation including dendritic and axonal growth, spine development, and synaptogenesis. We demonstrate that one brain-enriched microRNA, miR-137, has a significant role in regulating neuronal maturation. Overexpression of miR-137 inhibits dendritic morphogenesis, phenotypic maturation, and spine development both in brain and cultured primary neurons. On the other hand, a reduction in miR-137 had opposite effects. We further show that miR-137 targets the Mind bomb one (Mib1) protein through the conserved target site located in the 3' untranslated region of Mib1 messenger RNA. Mib1 is an ubiquitin ligase known to be important for neurodevelopment. We show that exogenously expressed Mib1 could partially rescue the phenotypes associated with miR-137 overexpression. These results demonstrate a novel miRNA-mediated mechanism involving miR-137 and Mib1 that function to regulate neuronal maturation and dendritic morphogenesis during development. STEM CELLS 2010;28:1060-1070
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