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Background  Notch signalling regulates neuronal differentiation in the vertebrate nervous system. In addition to a widespread function in maintaining neural progenitors, Notch signalling has also been involved in specific neuronal fate decisions. These functions are likely mediated by distinct Notch ligands, which show restricted expression patterns in the developing nervous system. Two ligands, in particular, are expressed in non-overlapping complementary domains of the embryonic spinal cord, with Jag1 being restricted to the V1 and dI6 progenitor domains, while Dll1 is expressed in the remaining domains. However, the specific contribution of different ligands to regulate neurogenesis in vertebrate embryos is still poorly understood.    Methodology/Principal Findings  In this work, we investigated the role of  Jag1  and  Dll1  during spinal cord neurogenesis, using conditional knockout mice where the two genes are deleted in the neuroepithelium, singly or in combination. Our analysis showed that  Jag1  deletion leads to a modest increase in V1 interneurons, while dI6 neurogenesis was unaltered. This mild  Jag1  phenotype contrasts with the strong neurogenic phenotype detected in  Dll1  mutants and led us to hypothesize that neighbouring Dll1-expressing cells signal to V1 and dI6 progenitors and restore neurogenesis in the absence of  Jag1 . Analysis of double  Dll1 ; Jag1  mutant embryos revealed a stronger increase in V1-derived interneurons and overproduction of dI6 interneurons. In the presence of a functional  Dll1  allele, V1 neurogenesis is restored to the levels detected in single  Jag1  mutants, while dI6 neurogenesis returns to normal, thereby confirming that  Dll1 -mediated signalling compensates for  Jag1  deletion in V1 and dI6 domains .Conclusions/Significance  Our results reveal that  Dll1  and  Jag1  are functionally equivalent in controlling the rate of neurogenesis within their expression domains. However, Jag1 can only activate Notch signalling within the V1 and dI6 domains, whereas Dll1 can signal to neural progenitors both inside and outside its domains of expression.

Two Notch Ligands, Dll1 and Jag1, Are Differently Restricted in Their Range of Action to Control Neurogenesis in the Mammalian Spinal Cord