Abstract

All components of the lateral line system (hair cells, neurons and ganglion cells) are derived from ectodermal thickenings called placodes. The posterior lateral line placode migrates from the head towards the tail tip where it deposits sensory organ precursor cells at regular intervals. Once developed, the functional unit of the lateral line (the neuromast) consists of relatively few cells. Throughout their embryonic and post-embryonic development, the primordia and the neuromasts are accessible to both experimental manipulations and live observations. Such relative simplicity and experimental accessibility make the lateral line system a unique model in which to study the complex cell-cell interactions that occur in the vertebrate nervous system. Yet, our understanding of the molecular mechanisms that regulate primordium migration and sensory organ deposition remains incomplete. We performed genetic screens and isolated approximately 20 mutants with different lateral line defects. Here we describe the phenotypic and molecular analysis of one of these mutants in which the primordium ceases to migrate prematurely and cell deposition is severely disrupted. Cloning of some of the other mutations has revealed that genes involved in lateral line development often participate in a variety of developmental processes in the embryo, such as cell migration, cell fate specification and patterning. These characteristics underscore the value of lateral line development as a tractable process, likely to inform fundamental aspects of vertebrate nervous system development.

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