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doi: 10.1242/10.1242/dev.00241
in populations of cranial and cardiac neural crest cells
Program in Developmental Biology and Division of Basic Sciences, Fred
Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA
98109, USA
* Present address: Department of Molecular Biology, University of Texas
Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9148,
USA
Author for correspondence (e-mail:
michelle.tallquist{at}utsouthwestern.edu)
Accepted 31 October 2002
Cardiac and cephalic neural crest cells (NCCs) are essential components of
the craniofacial and aortic arch mesenchyme. Genetic disruption of the
platelet-derived growth factor receptor 
(PDGFR) results in
defects in multiple tissues in the mouse, including neural crest derivatives
contributing to the frontonasal process and the aortic arch. Using chimeric
analysis, we show that loss of the receptor in NCCs renders them inefficient
at contributing to the cranial mesenchyme. Conditional gene ablation in NCCs
results in neonatal lethality because of aortic arch defects and a severely
cleft palate. The conotruncal defects are first observed at E11.5 and are
consistent with aberrant NCC development in the third, fourth and sixth
branchial arches, while the bone malformations present in the frontonasal
process and skull coincide with defects of NCCs from the first to third
branchial arches. Changes in cell proliferation, migration, or survival were
not observed in PDGFR NCC conditional embryos, suggesting that the
PDGFR may play a role in a later stage of NCC development. Our results
demonstrate that the PDGFR plays an essential, cell-autonomous role in
the development of cardiac and cephalic NCCs and provides a model for the
study of aberrant NCC development.
Key words: Chimeric analysis, Cre-loxP recombination, Neural crest, PDGF receptor, Mouse
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