Extending this principle to neurogenesis, in the murine retina, conditional inactivation of Notch1 or CBF1 showed that pathway activity is required to suppress photoreceptor fate by first inhibiting cone generation, and later, rod generation (Jadhav et al., 2006, Riesenberg et al., 2009, Yaron et al., 2006 and Zheng et al., 2009). These findings were of particular interest Selleckchem Ferroptosis inhibitor because they revealed that Notch signaling was preferentially suppressing photoreceptor fate rather than all neuronal fates, which would have been the simplest prediction if Notch were primarily maintaining progenitor character. Consistent with a role in generating
neuronal subtype diversity, recently it has been shown that Notch signaling in vertebrates can regulate binary fate choices leading to multiple distinct neuronal cell types (Cau and Blader, 2009). Such a function for Notch is consistent with its long-appreciated role in binary fate choices in invertebrates, in particular nematode vulval development, and Drosophila PNS and eye development ( Sundaram, 2005). For example, in the spinal cord Notch was shown to influence the generation of excitatory
and inhibitory interneurons in both the dorsal and ventral domains. Interestingly, Notch promoted excitatory interneuron character dorsally ( Mizuguchi et al., 2006), and inhibitory click here interneuron character ventrally ( Peng et al., 2007), indicating that Notch
activity is not instructively generating neurons of a specific neurotransmitter type, and is instead acting in a context-dependent manner. Similar findings have been obtained in work on the zebrafish spinal cord, suggesting that a role for Notch in regulating spinal cord neuronal subtype identity is evolutionarily conserved ( Batista et al., 2008 and Kimura et al., 2008). Another example of the Notch pathway playing a role during a binary mafosfamide fate choice can be found in studies of the inner ear (Cotanche and Kaiser, 2010). In the developing cochlea, prosensory patches are first specified by Notch activation using an inductive mechanism (Daudet and Lewis, 2005 and Hartman et al., 2010). Expression of the Notch ligand Jag1 in clusters of cells leads to Notch receptor activation, and the subsequent expression of the transcription factor Sox2, which together with Notch signaling plays an essential role in prosensory patch establishment and maintenance (Daudet et al., 2007, Daudet and Lewis, 2005 and Kiernan et al., 2005b). Subsequent to the formation of such patches, the Notch pathway is again deployed to mediate the division of the prosensory patch into a cellular mosaic composed of sensory hair cells and supporting cells.
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