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First published online 12 October 2005
doi: 10.1242/dev.02072
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1 Department of Biochemistry and Molecular Biology, Norris Cancer Hospital, Keck
School of Medicine, University of Southern California, 1441 Eastlake Avenue,
Los Angeles, CA 90089, USA
2 Center for Craniofacial Molecular Biology, School of Dentistry, University of
Southern California, 2250 Alcazar Street, CSA 103, Los Angeles, CA 90033,
USA
* Author for correspondence (e-mail: maxson{at}hsc.usc.edu)
Accepted 2 September 2005
The neural crest is a multipotent, migratory cell population that
contributes to a variety of tissues and organs during vertebrate
embryogenesis. Here, we focus on the function of Msx1 and
Msx2, homeobox genes implicated in several disorders affecting
craniofacial development in humans. We show that Msx1/2
mutants exhibit profound deficiencies in the development of structures derived
from the cranial and cardiac neural crest. These include hypoplastic and
mispatterned cranial ganglia, dysmorphogenesis of pharyngeal arch derivatives
and abnormal organization of conotruncal structures in the developing heart.
The expression of the neural crest markers Ap-2
,
Sox10 and cadherin 6 (cdh6) in Msx1/2
mutants revealed an apparent retardation in the migration of subpopulations of
preotic and postotic neural crest cells, and a disorganization of neural crest
cells paralleling patterning defects in cranial nerves. In addition, normally
distinct subpopulations of migrating crest underwent mixing. The expression of
the hindbrain markers Krox20 and Epha4 was altered in
Msx1/2 mutants, suggesting that defects in neural crest
populations may result, in part, from defects in rhombomere identity.
Msx1/2 mutants also exhibited increased Bmp4
expression in migratory cranial neural crest and pharyngeal arches. Finally,
proliferation of neural crest-derived mesenchyme was unchanged, but the number
of apoptotic cells was increased substantially in neural crest-derived cells
that contribute to the cranial ganglia and the first pharyngeal arch. This
increase in apoptosis may contribute to the mispatterning of the cranial
ganglia and the hypoplasia of the first arch.
Key words: Neural Crest, Calvaria, Craniofacial, Cranial Ganglia, Cardiac outflow tract, Msx1, Msx2, Mouse embryo
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