Journal
DEVELOPMENTAL BIOLOGY
Volume 411, Issue 1, Pages 85-100Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2016.01.006
Keywords
Hedgehog; Notch; Gli transcription factors; Gli2; Retinal histogenesis; Neural progenitor; Muller glia; Competency; Proliferation
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Funding
- Canadian Institutes of Health Research [189928]
- Canadian Cancer Society [2010-700508]
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Neurogenesis is regulated by the dynamic and coordinated activity of several extracellular signalling pathways, but the basis for crosstalk between these pathways remains poorly understood. Here we investigated regulatory interactions between two pathways that are each required for neural progenitor cell maintenance in the postnatal retina; Hedgehog (Hh) and Notch signalling. Both pathways are activated in progenitor cells in the postnatal retina based on the co-expression of fluorescent pathway reporter transgenes at the single cell level. Disrupting Notch signalling, genetically or pharmacologically, induces a rapid downregulation of all three Gli proteins and inhibits Hh-induced proliferation. Ectopic Notch activation, while not sufficient to promote Hh signalling or proliferation, increases Gli2 protein. We show that Notch regulation of Gli2 in Muller glia renders these cells competent to proliferate in response to Hh. These data suggest that Notch signalling converges on Gli2 to prime postnatal retinal progenitor cells and Muller glia to proliferate in response to Hh. (C) 2016 Elsevier Inc. All rights reserved.
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