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Shh/Boc signaling is required for sustained generation of ipsilateral projecting ganglion cells in the mouse retina

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dc.contributor.author Sánchez-Arrones, Luisa spa
dc.contributor.author Nieto-Lopez, Francisco spa
dc.contributor.author Sánchez-Camacho Blázquez, Cristina spa
dc.contributor.author Carreres, M. Isabel spa
dc.contributor.author Herrera, Eloisa spa
dc.contributor.author Okada, Ami spa
dc.contributor.author Bovolenta, Paola spa
dc.date.accessioned 2013-11-27T17:26:43Z
dc.date.available 2013-11-27T17:26:43Z
dc.date.issued 2013 spa
dc.identifier.citation Sánchez-Arrones, L., Nieto-López, F., Sánchez-Camacho, C., Carreres, M. I., Herrera, E., Okada, A., & Bovolenta, P. (2013). Shh/Boc signaling is required for sustained generation of ipsilateral projecting ganglion cells in the mouse retina. The Journal of Neuroscience, 33(20), 8596-8607. spa
dc.identifier.uri http://hdl.handle.net/11268/993
dc.description.abstract Sonic Hedgehog (Shh) signaling is an important determinant of vertebrate retinal ganglion cell (RGC) development. In mice, there are two major RGC populations: (1) the Islet2-expressing contralateral projecting (c)RGCs, which both produce and respond to Shh; and (2) the Zic2-expressing ipsilateral projecting RGCs (iRGCs), which lack Shh expression. In contrast to cRGCs, iRGCs, which are generated in the ventrotemporal crescent (VTC) of the retina, specifically express Boc, a cell adhesion molecule that acts as a high-affinity receptor for Shh. In Boc −/− mutant mice, the ipsilateral projection is significantly decreased. Here, we demonstrate that this phenotype results, at least in part, from the misspecification of a proportion of iRGCs. In Boc−/− VTC, the number of Zic2-positive RGCs is reduced, whereas more Islet2/Shh-positive RGCs are observed, a phenotype also detected in Zic2 and Foxd1 null embryos. spa
dc.language.iso eng spa
dc.title Shh/Boc signaling is required for sustained generation of ipsilateral projecting ganglion cells in the mouse retina spa
dc.type article spa
dc.description.impact 6.747 JCR (2013) Q1, 24/251 Neurosciences spa
dc.identifier.doi 10.1523/JNEUROSCI.2083-12.2013 spa
dc.rights.accessRights closedAccess en
dc.subject.unesco Oftalmología spa
dc.subject.unesco Genética humana spa
dc.peerreviewed Si spa


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