|
|
|
Associate Professor
Current Funding"Molecular Mechanisms of Mouse Mesoderm Differentiation", Carol Burdsal, PI, NIH, 1998 to 2000. Click here to read a summary of this project. "Cell Differentiation During Craniofacial Development," Carol Burdsal, PI, Millennium Trust Human Excellence Fund Grant, Louisiana Board of Regents, 2000 to 2005. Click here to read a summary of this project. "Retinoid Signaling", Carol Burdsal, PI, Environmental Sensors and Signals, Tulane/Xavier Center for Bioenvironmental Research, 2000 to 2005. Click here to read a summary of this project. Molecular Mechanisms of Mouse Mesoderm Differentiation A vital mechanism that gives form and pattern to the vertebrate embryo is embryonic induction, the process by which one cell influences the differentiation and/or behavior of another. In vertebrates, a complex network of peptide growth factors has been shown to induce and pattern the differentiation of mesoderm. The studies proposed here will address two general questions: first, how signals mediated by peptide growth factors are integrated to produce the ordered differentiation of mesoderm in the mouse embryo, and second, the role played by protein phosphatases which modulate signal transduction pathways during mesoderm induction in the mouse. Cell Differentiation During Craniofacial Development Cleft lip, with or without cleft palate (cleft lip/palate), is one of the most common human birth defects occurring at a frequency of 1/700 live births. Craniofacial defects like cleft lip/palate occur when the timing, rate, or extent of outgrowth of the facial primordia is interrupted during embryogenesis and this type of birth defect has an estimated economic cost in the United States of $697,000,000 (Centers for Disease Control and Prevention, 1995). Elucidating the molecular mechanisms that regulate normal fusion and differentiation in craniofacial tissues is vital for devising strategies to prevent the burden this type of defect places on families and on the US health care system. We have identified a novel transcriptional activator, named Pigpen, that is essential for cell proliferation, that is expressed in the craniofacial mesenchyme in mouse and chick embryos, and that is regulated by fibroblast growth factor-8 (FGF-8) signals during the epithelial-mesenchymal interactions which are known guide craniofacial morphogenesis. The goal of this study is to determine the role Pigpen plays in regulating cell growth, differentiation, and patterning during vertebrate craniofacial development. All-trans-retinoic acid (RA) is required for successful embryonic development in vertebrates, but exposure to too high a level of RA causes birth defects. Therefore, quantitative control of the levels of RA in the vertebrate embryo is necessary for correct embryonic development. Recently, enzymes capable of catabolizing RA were found to constitute a new family, called CYP26, within the cytochrome P450 superfamily. CYP26 homologues have been isolated from human, mouse, zebra fish and recently from the chick. Because CYP26 activity can reduce the level of RA in embryonic tissues, this gene product may play an important regulatory role in vertebrate embryogenesis. The purpose of this study is to determine if and how CYP26 regulates embryonic development in vertebrates and if it acts as a signal for retinoid-like molecules found in the environment. Courses Taught
CELL
471/671, Molecular Biology of Cancer |
|