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. 2022 May 18;10:887764. doi: 10.3389/fcell.2022.887764

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Copyright © 2022 Hanna, David, Touahri, Fleming, Screaton and Schuurmans.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Notch signaling and lateral inhibition. Notch signaling sustains RPC proliferation and prevents differentiation via its downstream effectors, Hes1 and Hes5. The cell that becomes a Müller glia expresses high levels of the Notch receptor, which is stimulated by a Delta ligand (Dll1) on the neighboring cell. The Notch intracellular domain (NICD) is then cleaved, translocates to the nucleus, and binds Rbpj to initiate the transcription of Hes1 and Hes5. Hes1 and Hes5 repress the transcription of Ascl1. This process initiates Müller glia specification and represses differentiation, including a photoreceptor fate.