期刊
DEVELOPMENTAL CELL
卷 27, 期 2, 页码 174-187出版社
CELL PRESS
DOI: 10.1016/j.devcel.2013.09.018
关键词
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资金
- Ramon y Cajal [RyC-2010-07155]
- Ministerio de Economia y Competitividad [SAF2012-31467]
- National Institutes of Health [R01 EY017916]
- Spanish National grants [BFU2009-09074, SAF2012-35181]
- Generalitat Valenciana grant [PROMETEO II/2013/001]
- Fundacion Botin
Neuroepithelial cell proliferation must be carefully balanced with the transition to neuroblast (neural stem cell) to control neurogenesis. Here, we show that loss of the Drosophila microRNA mir-8 (the homolog of vertebrate miR-200 family) results in both excess proliferation and ectopic neuroblast transition. Unexpectedly, mir-8 is expressed in a subpopulation of optic-lobe-associated cortex glia that extend processes that ensheath the neuroepithelium, suggesting that glia cells communicate with the neuroepithelium. We provide evidence that miR-8-positive glia express Spitz, a transforming growth factor alpha (TGF-alpha)-like ligand that triggers epidermal growth factor receptor (EGFR) activation to promote neuroepithelial proliferation and neuroblast formation. Further, our experiments suggest that miR-8 ensures both a correct glial architecture and the spatiotemporal control of Spitz protein synthesis via direct binding to Spitz 3' UTR. Together, these results establish glial-derived cues as key regulatory elements in the control of neuroepithelial cell proliferation and the neuroblast transition.
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