Associate Professor
Ph.D. (1989) University of California, Berkeley

Contact

bcondie@uga.edu
  • Grant Support -
  • Research Interests -
    • A major goal of the research in my lab is define the genetic pathways that regulate fetal thymus development in mice.  Normal thymus development is necessary for the production of normal T cells - the key components of cellular adaptive immunity in mammals.  We are focused on defining the pathways that regulate the differentiation of thymic epithelial cells (TECs) from the pharyngeal endoderm.  TECs provide the  microenvironment that is required for normal T cell production from lymphoid progenitor cells.  Although TECs play a critical role in normal T cell production there is relatively little known about their normal development.  To address this gap in knowledge my lab has recently identified several candidate transcription factors that are involved in TEC differentiation and genetic studies of these factors in mice are underway.  The genes we are identifying are candidates for loci involved in causing T cell immunodeficiencies or dysfunction.  They will also be important for future studies of thymus aging and regeneration.

      I also have a strong interest in developing new genetic research tools that are based on site-specific recombination.  Site-specific recombinases are used to generate tissue specific genetic modifications in mice and other systems.  I am focused on developing new approaches for tissue or cell type restricted activation of site-specific recombinases in developing and adult mice as well as in cultured stem cells.

Selected Publications:
  • Condie, B. G. and Urbanski, W. M. (2014)  Using the Textpresso Site Specific Recombinases web server to identify Cre expressing mouse strains and floxed alleles.  Methods in Molecular Biology 1092, 395-403.
  • Casoni, F., Hutchins, B.I., Donohue, D., Fornaro, M., Condie, B.G. and Wray, S. (2012). SDF and GABA Interact to Regulate Axophilic Migration of GnRH-1 Neurons.  Journal of Cell Science 125, 5015-5025.
  • Manley, N.R., Richie E.R., Blackburn, C.C., Condie, B.G., and Sage, J. (2011). Structure and function of the thymic microenvironment.  Frontiers in Bioscience 17, 2461-2477.
  • Wei Q., Manley, N.R. and Condie B.G. (2011). Whole mount in situ hybridization of E8.5-E11.5 mouse embryos.  J. Vis. Exp.  e2797 doi: 10.3791/2797, pubmed id 22005971.
  • Wei, Q. and Condie B.G. (2011) A focused in situ hybridization screen identifies candidate transcriptional regulators of thymic epithelial cell development and function.  Plos One 6, 26795.
  • Guo, T., Mandai, K., Condie, B.G., Wickramasinghe, R.S., Capecchi, M.R. and Ginty, D.D. (2011). An evolving NGF-Hoxd1 signaling pathway mediates development of divergent neural circuits in vertebrates.  Nature Neuroscience 14, 31-36.
  • Manley, N.R. and B.G. Condie. 2010. Transcriptional regulation of thymus organogenesis and thymic epithelial cell differentiation. Progress in Molecular Biology and Translational Science 92C: 103-120.
  • Chen, L., P. Zhao, L. Wells, C.T. Amemiya, B.G. Condie and Manley, N.R. 2010. Mouse and zebrafish Hoxa3 orthologs have non-equivalent in vivo protein function. PNAS 107: 10555-10560.
  • Oh, W.-J., J.J. Westmoreland, R. Summers and B.G. Condie. 2010. Cleft palate and body wall defects are caused by CNS dysfunction in Gad1 and Viaat knockout mice. PLoS One 5: e9758.
  • Urbanski, W.M. and B.G. Condie. 2009. Textpresso Site-Specific Recombinases: a text-mining server for the recombinase literature including Cre mice and conditional alleles. Genesis 47: 842-846.
  • Lee J.M., J. Tiong, D.M. Maddox, B.G. Condie and S. Wray. 2008. Temporal migration of GnRH-1 neurones is modified in GAD67 knockout mouse. J. Neuroendocrinology 20: 93-103.
  • Gordon, J., B. Hughes, D.-M. Su, S. Xiao, S.P. Navarre, B.G. Condie and N.R. Manley. 2007. Specific expression of lacZ and Cre recombinase in fetal thymic epithelial cells by multiplex gene targeting at the Foxn1 locus. BMC Developmental Biology 7: 69.
  • Noggle, S.A., D. Weiler and B.G. Condie. 2006. NOTCH signaling is inactive but inducible in human embryonic stem cells. Stem Cells 24: 1646-1653.
  • Oh, W.-J., S.A. Noggle, D.M. Maddox and B.G. Condie. 2005. The mouse Viaat/Vgat gene: expression during embryogenesis, analysis of its core promoter in neural stem cells and a reconsideration of its alternate splicing. Gene 351: 39-49.
  • Bieberich, E., J. Silva, G. Wang, K. Krishnamurthy and B.G. Condie. 2004. Selective apoptosis of pluripotent mouse and human stem cells by novel ceramide analogs prevents teratoma formation and enriches for neural precursors in ES-cell derived neural transplants. J. Cell Biology 167: 723-734.