Dr. Amy Sater's lab seeks to understand the processes by which ectodermal cells become committed to form epidermis, neurons, or glia during embryonic development of the African Clawed Frog, Xenopus laevis. One current project investigates the roles of microRNAs (miRs) in the regulation of ectodermal specification. The lab has identified miRs and miR-targeted RNAs in early neural and epidermal ectoderm and are now testing functions of selected miR-mRNA interactions in the regulation of cell fate.
A second study addresses mechanisms of astrocyte specification and the maintenance of developmental plasticity in astrocytes. Although proliferating neural progenitors acquire the capacity to initiate glial development well after the initiation of neurogenesis, the molecular basis of this "gliogenic switch," and the paracrine signals and gene regulatory networks that govern the progression from neural progenitor to differentiated astrocyte are poorly understood. The Sater Lab combines genetic, embryological, and genomic approaches to understand the molecular control of astrocyte development.
The Sater Lab has recently begun a new project to develop Xenopus tadpoles as a model system for the investigation of astrocyte responses to traumatic brain injury (TBI). The working hypothesis is that modulation of astrocyte responses to TBI could promote neural regeneration and repair by improving the microenvironment. The lab is currently developing transgenic reporter lines so that astrocyte responses to injury can be monitored in vivo using live imaging. One long-term goal of this project is to use our reporter lines to carry out pharmacological screens for compounds that either reduce the pro-inflammatory response, or promote a neuroprotective, or "pro-regeneration," response.
Publications/Creative Works
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