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Dev Cell. 2013 Oct 28;27(2):174-187. doi: 10.1016/j.devcel.2013.09.018. Epub 2013 Oct 17.

Conserved miR-8/miR-200 defines a glial niche that controls neuroepithelial expansion and neuroblast transition.

Author information

1
Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas y Universidad Miguel Hernández, Av Santiago Ramón y Cajal s/n, 03550 San Juan de Alicante, Spain. Electronic address: j.morante@umh.es.
2
Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas y Universidad Miguel Hernández, Av Santiago Ramón y Cajal s/n, 03550 San Juan de Alicante, Spain.
3
Center for Developmental Genetics, Department of Biology, New York University, 100 Washington Square East, New York, NY 10003, USA.

Abstract

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 α (TGF-α)-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.

PMID:
24139822
PMCID:
PMC3931912
DOI:
10.1016/j.devcel.2013.09.018
[Indexed for MEDLINE]
Free PMC Article

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