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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

mlcondic@neuro.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 collaborating with a team of developmental biologists and pediatric cardiologists to investigate the stem cell properties of human amniocytes, and determine whether these cells can be differentiated into cardiac and neural lineages in vitro, as a possible  approach to both diagnostics and therapeutic treatment of congenital heart disease. 

The final area of research in the laboratory involves 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. 

We are currently investigating the role of netrin-1 and cAMP signaling pathways in regulating growth cone motility and guidance.   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