J C Minarcik1, J A Golden. 1. Department of Pathology, Children's Hospital of Philadelphia, PA 19104, USA.
Abstract
OBJECTIVE: To determine if distinct populations of cranial neural crest cells (CNCC) exist by characterization of their divergent gene expression patterns. DESIGN: Identification of unique populations of CNCC was determined by a combination of lineage and immunohistochemical analyses. SETTING: Department of Pathology, Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, PA 19104. RESULTS: We found antibodies of two proteins previously described as identifying all CNCC, label three populations of CNCC at specific time-points. Furthermore, the activating protein 2 (AP-2) expressing CNCC become neural or mesenchymal NCC derivatives whereas the HNK-1 labeled cells do not participate in the mesenchymal lineage. CONCLUSION: These data provide molecular markers for unique CNCC fates and thus will be invaluable in the characterizing of craniofacial anomalies related to defects in NCCS. In addition, our data suggest AP-2 may function in determining the unique mesenchymal fate of CNCCs.
OBJECTIVE: To determine if distinct populations of cranial neural crest cells (CNCC) exist by characterization of their divergent gene expression patterns. DESIGN: Identification of unique populations of CNCC was determined by a combination of lineage and immunohistochemical analyses. SETTING: Department of Pathology, Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, PA 19104. RESULTS: We found antibodies of two proteins previously described as identifying all CNCC, label three populations of CNCC at specific time-points. Furthermore, the activating protein 2 (AP-2) expressing CNCC become neural or mesenchymal NCC derivatives whereas the HNK-1 labeled cells do not participate in the mesenchymal lineage. CONCLUSION: These data provide molecular markers for unique CNCC fates and thus will be invaluable in the characterizing of craniofacial anomalies related to defects in NCCS. In addition, our data suggest AP-2 may function in determining the unique mesenchymal fate of CNCCs.
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