JOINT SEMINARS IN NEUROSCIENCE
TUESDAY, FEBRUARY 9nd, 2016 AT 12:00 NOON
Speaker: GREG BASHAW, PhD, Professor
Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Host: SAMANTHA BUTLER, PhD, Assistant Professor
Department of Neurobiology, UCLA
Title: "To cross or not to cross: molecular mechanisms that regulate axon guidance at the midline"
12:00pm Neuroscience Research Building (NRB) Auditorium, UCLA
Dr Bashaw's research explores a fundamental problem in neurobiology: how axons in the developing nervous system successfully navigate to their correct targets. Understanding the mechanisms that mediate axon guidance provides important insight into how the nervous system is correctly wired during development and may have implications for therapeutic approaches to developmental brain disorders and nerve regeneration. Achieving this understanding requires unraveling the molecular logic that ensures the proper expression and localization of axon guidance cues and receptors, and elucidating the signaling events that regulate the growth cone cytoskeleton in response to guidance receptor activation.
Research in Dr Bashaw's laboratory addresses the dynamics of axon guidance receptor expression and signaling, and exploits the powerful genetic and molecular approaches available in Drosophila. In particular, the group studies the Slit ligand and Roundabout receptors, and the Netrin ligand and DCC/UNC5 receptors -- two important evolutionary conserved ligand/receptor systems that contribute to proper connectivity in both the vertebrate and invertebrate nervous systems. These molecules are also known to influence neuronal and mesodermal cell migration, suggesting that determining their function may have broad implications for understanding diseases of nervous system development, many of which have their root in defective cell migration and/or axon guidance.
Dr Bashaw has also discovered that in addition to its canonical role in signaling locally to regulate growth cone movement and morphology, the Frazzled/DCC receptor can also act as a transcription factor to regulate gene expression. In this context, the receptor is cleaved to generate a soluble intracellular domain that can translocate to the nucleus where it activates transcription of key target genes.