Abstract
sox10 is necessary for development of neural and pigment cell derivatives of the neural crest (NC). However, whereas a direct role for Sox10 activity has been established in pigment and glial lineages, this is more controversial in NC-derived sensory neurons of the dorsal root ganglia (DRGs). We proposed that sox10 functioned in specification of sensory neurons, whereas others suggested that sensory neuronal defects were merely secondary to absence of glia. Here we provide evidence that in zebrafish, early DRG sensory neuron survival is independent of differentiated glia. Critically, we demonstrate that Sox10 is expressed transiently in the sensory neuron lineage, and specifies sensory neuron precursors by regulating the proneural gene neurogenin1. Consistent with this, we have isolated a novel sox10 mutant that lacks glia and yet displays a neurogenic DRG phenotype. In conjunction with previous findings, these data establish the generality of our model of Sox10 function in NC fate specification.
Highlights
In the trunk and tail, sensory neurons are clustered with support cells to form a reiterated segmental series of dorsal root ganglia (DRGs) (Le Douarin and Kalcheim, 1999)
We recently proposed, based in part on single-cell analysis of NC cells (NCCs) in sox10 mutants, that zebrafish sox10 has a primary role in NCC fate specification, in all neuronal, glial and pigment cell lineages (Dutton et al, 2001b; Kelsh and Raible, 2002)
Primary versus secondary loss of sensory neurons in sox10 mutants Studies of the Sox10 mutant DRG phenotype at trunk axial levels in mouse showed that nascent DRG size was approximately normal at E10, subsequently the constituent NCCs failed to show any glial cell markers, showed reduced DRG neurons, and later lost motorneurons (Britsch et al, 2001; Sonnenberg-Riethmacher et al, 2001)
Summary
In the trunk and tail, sensory neurons are clustered with support cells (glia) to form a reiterated segmental series of dorsal root ganglia (DRGs) (Le Douarin and Kalcheim, 1999). Complete lack of Sox function results in cell death before overt fate acquisition, and any surviving cells fail to subsequently differentiate as glia (Britsch et al, 2001; Kapur, 1999; Paratore et al, 2001). Consistent with these defects, in mammals and in chick, Sox is expressed in undifferentiated NC and persistently in mature
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