Search

• Sensory neurons in the dorsal root ganglia arise from trunk neural crest cells. • A diversity of guidance cues orchestrate sensory axon targeting. • High degree of conservation of molecular pathways regulating sensory neuron development. • Insightful divergences of sensory types in aquatic vs. terrestrial vertebrates. Crucial to an animal's movement through their environment and to the maintenance of their homeostatic physiology is the integration of sensory information. This is achieved by axons communicating from organs, muscle spindles and skin that connect to the sensory ganglia composing the peripheral nervous system (PNS), enabling organisms to collect an ever-constant flow of sensations and relay it to the spinal cord. The sensory system carries a wide spectrum of sensory modalities – from sharp pain to cool refreshing touch – traveling from the periphery to the spinal cord via the dorsal root ganglia (DRG). This review covers the origins and development of the DRG and the cells that populate it, and focuses on how sensory connectivity to the spinal cord is achieved by the diverse developmental and molecular processes that control axon guidance in the trunk sensory system. We also describe convergences and differences in sensory neuron formation among different vertebrate species to gain insight into underlying developmental mechanisms. [ABSTRACT FROM AUTHOR]

The formation of the vertebrate nervous system depends on the complex interplay of morphogen signaling pathways and cell cycle progression to establish distinct cell fates. The Sonic hedgehog (Shh) signaling pathway is well understood to promote ventral cell fates in the developing spinal cord. A key regulator of Shh signaling is its receptor Patched1 (Ptch1). However, because the Ptch1 null mutation is lethal early in mouse embryogenesis, its role in controlling cell cycle progression, neurogenesis, and axon guidance in the developing spinal cord is not fully understood. An allele of Ptch1 called Wiggable (Ptch1 Wig ), which was previously shown to enhance Shh signaling, was used to test its ability to regulate neurogenesis and proliferation in the developing spinal cord. Ptch1 Wig/Wig mutants displayed enhanced ventral proneural gene activation, and aberrant proliferation of the neural tube and floor plate cells, the latter normally being a quiescent population. The expression of the cell cycle regulators p27Kip1 and p57Kip2 were expanded in Ptch1 Wig/Wig mutant spinal cords, as was the number of mitotic and S-phase nuclei, suggesting enhanced cell cycle progression. However, Ptch1 Wig/Wig mutants also showed enhanced apoptosis in the ventral embryonic spinal cord, which resulted in thinner spinal cords at later embryonic stages. Commissural axons largely failed to cross the floor plate of Ptch1 Wig/Wig mutant embryos, suggesting enhanced Shh signaling in these mutants led to a dorsal expansion of the chemoattraction front. These findings are consistent with a role of Ptch1 in regulating neurogenesis and proliferation of neural progenitors, and in restricting the influence of Shh signaling in commissural axon guidance to the floor plate. • Patched1 (Ptch1) regulates proliferation and neurogenesis in the ventral embryonic spinal cord. • The Ptch1 Wig mutation, which produced a truncated Ptch1 receptor protein, resulted in the aberrant proliferation of floor plate cells. • Ptch1 Wig mutants displayed aberrant targeting of commissural neurons and a general failure to cross the midline. [ABSTRACT FROM AUTHOR]