2008 OSU Molecular Life Sciences
Interdisciplinary Graduate Programs Symposium
Poster abstracts
Abstract:
Neural crest cells give rise to numerous derivatives including chromatophores, craniofacial cartilages, and neurons and glia of the peripheral nervous system. Likewise, lateral plate mesoderm generates numerous blood, cardiac and vascular derivatives. The genetic control of neural crest and lateral plate mesoderm development are incompletely understood. hatchback (hbk) is an ENU-induced recessive embryonic lethal mutation that was identified based on the near absence of trunk neural crest cells in mutant embryos. All chromatophores are absent or nearly absent in hbk mutants. Sympathetic, dorsal root ganglion and enteric neurons are also missing. The absence of neural crest-derivatives is preceded by abnormal expression of multiple transcription factors known to regulate early neural crest development. hbk mutant embryos also display defects in cardiovascular development as evidenced by cardiac edema and a lack of blood and circulation. Abnormal expression of several genes known to regulate the development of cardiac, vascular and hematopoietic progenitors has also been observed. Neural plate and axial and paraxial mesoderm development in hbk mutants is indistinguishable from wild-type siblings. These observations suggest hbk function is specifically required for neural crest induction and/or early development, as well as for the establishment and development of specific lateral plate mesoderm-derived lineages.
Keywords: neural crest, lateral mesoderm