Abstract
The Slit/Robo axon guidance families play a vital role in the formation of neural circuitry within select regions of the developing mouse nervous system. Typically Slits signal through the Robo receptors, however they also have Robo-independent functions. The novel Slit receptor Eva-1, recently discovered in C. elegans, and the human orthologue of which is located in the Down syndrome critical region on chromosome 21, could account for some of these Robo independent functions as well as provide selectivity to Robo-mediated axon responses to Slit. Here we investigate the expression of the mammalian orthologue EVA1C in regions of the developing mouse nervous system which have been shown to exhibit Robo-dependent and -independent responses to Slit. We report that EVA1C is expressed by axons contributing to commissures, tracts and nerve pathways of the developing spinal cord and forebrain. Furthermore it is expressed by axons that display both Robo-dependent and -independent functions of Slit, supporting a role for EVA1C in Slit/Robo mediated neural circuit formation in the developing nervous system.
Highlights
The Slit/Robo families are chemorepulsive cues that were first identified in Drosophila, where they are most well-known for regulation of midline crossing by commissural axons [1]
EVA1C is Expressed in Embryonic Spinal Cord Spinal commissural neurons project axons across the floor plate into the contralateral ventrolateral funiculus in a process tightly controlled by Slit/Robo signaling [8,15,16]
At E17.5, EVA1C was clearly expressed in the ascending and descending longitudinal pathways that constitute the dorsal columns (DC, Fig. 1E), dorsal funiculus (DF, Fig. 1D) and ventrolateral funiculus (VLF, Fig. 1F)
Summary
The Slit/Robo families are chemorepulsive cues that were first identified in Drosophila, where they are most well-known for regulation of midline crossing by commissural axons [1]. The axon guidance function of Slit/Robo signaling is highly conserved in mice and humans and appears to be associated with some neurological disorders. Defects in Slit/Robo signaling disrupt commissural axon crossing in the hindbrain in horizontal gaze palsy with progressive scoliosis [4,5]. While the Slits primarily signal through the Robo receptors, they have Robo-independent functions in the guidance of spinal commissural, cortical and olfactory axons [8,9,10]. This has led to the proposal that a new Slit receptor exists in mice, which acts either in conjunction or independently of Robos to regulate guidance
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