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Maureen L. Condic

Associate Professor of Neurobiology and Anatomy

B.A. University of Chicago

Ph.D. University of California, Berkeley

Research

References

maureen.condic@hsc.utah.edu

Maureen Condic's PubMed Literature Search

Research

The factors controlling specification of neuronal identity in the peripheral nervous system   are poorly understood.    We have recently shown that sensory neurons are distinct prior to target enervation and characterized early differences in gene expression and growth cone motility between different classes of sensory neurons.   We are currently investigating the role of the Hedgehog and BMP signaling pathways in the specification of sensory neuron phenotype, both in vivo and in vitro.   In a related body of work, we are investigating the interactions of different classes of developing sensory neurons with the extracellular matrix as they extend towards their targets.   We have shown that neurons regulate the transcription,   subcellular localization and the functional state of matrix receptors (receptors of the integrin class) in ways that other cells do not.   Regulation of integrin expression and function enables embryonic neurons to compensate for the diverse embryonic environments sensory growth cones must traverse during development, including tissues that express low levels of growth promoting molecules and/or growth-inhibiting molecules.   Increasing integrin expression in neurons is sufficient to promote efficient regeneration of both embryonic and adult neurons in the presence of molecules that normally inhibit axon extension.   The ability of altered integrin expression and/or function to promote axonal regeneration in vivo is currently being investigated.   We have extended our observations on sensory growth cone migration to a second population of "invasive" cells, the embryonic neural crest.   Neural crest cells migrate extensively through the embryo to give rise to a wide range of derivatives, including sensory neurons.   We have demonstrated that neural crest cells also regulate their motility to compensate for diverse extracellular conditions.  

The cell biology of neural crest migration and the interaction between crest motility and specification of crest fates during development are currently under investigation.

Adult rat sensory neurons cultured on a weakly permissive substrata, similar to the extracellular environment of the adult central nervous system. A control neuron (red) infected with an adenoviral construct expressing beta-galactosidase shows the poor axon extension characteristic of regenerating adult neurons. In contrast, a neuron infected with adenovirus expressing the integrin receptor alpha5b1 (green) shows robust regeneration under the same conditions.

References