scholarly journals Hand1 phosphoregulation within the distal arch neural crest is essential for craniofacial morphogenesis

Development ◽  
2014 ◽  
Vol 141 (15) ◽  
pp. 3050-3061 ◽  
Author(s):  
B. A. Firulli ◽  
R. K. Fuchs ◽  
J. W. Vincentz ◽  
D. E. Clouthier ◽  
A. B. Firulli
Keyword(s):  
Neural Crest ◽  
Arch Neural ◽  
Craniofacial Morphogenesis

sucker encodes a zebrafish Endothelin-1 required for ventral pharyngeal arch development

Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3815-3828 ◽  
Author(s):  
C.T. Miller ◽  
T.F. Schilling ◽  
K. Lee ◽  
J. Parker ◽  
C.B. Kimmel
Keyword(s):  
Neural Crest ◽  
Expression Patterns ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Dorsoventral Patterning ◽  
Surface Ectoderm ◽  
Pharyngeal Arches ◽  
Endothelin 1 ◽  
Lower Jaw ◽  
Arch Neural

Mutation of sucker (suc) disrupts development of the lower jaw and other ventral cartilages in pharyngeal segments of the zebrafish head. Our sequencing, cosegregation and rescue results indicate that suc encodes an Endothelin-1 (Et-1). Like mouse and chick Et-1, suc/et-1 is expressed in a central core of arch paraxial mesoderm and in arch epithelia, both surface ectoderm and pharyngeal endoderm, but not in skeletogenic neural crest. Long before chondrogenesis, suc/et-1 mutant embryos have severe defects in ventral arch neural crest expression of dHAND, dlx2, msxE, gsc, dlx3 and EphA3 in the anterior arches. Dorsal expression patterns are unaffected. Later in development, suc/et-1 mutant embryos display defects in mesodermal and endodermal tissues of the pharynx. Ventral premyogenic condensations fail to express myoD, which correlates with a ventral muscle defect. Further, expression of shh in endoderm of the first pharyngeal pouch fails to extend as far laterally as in wild types. We use mosaic analyses to show that suc/et-1 functions nonautonomously in neural crest cells, and is thus required in the environment of postmigratory neural crest cells to specify ventral arch fates. Our mosaic analyses further show that suc/et-1 nonautonomously functions in mesendoderm for ventral arch muscle formation. Collectively our results support a model for dorsoventral patterning of the gnathostome pharyngeal arches in which Et-1 in the environment of the postmigratory cranial neural crest specifies the lower jaw and other ventral arch fates.

Role of Dlx-1 and Dlx-2 genes in patterning of the murine dentition

Development ◽  
1997 ◽  
Vol 124 (23) ◽  
pp. 4811-4818 ◽  
Author(s):  
B.L. Thomas ◽  
A.S. Tucker ◽  
M. Qui ◽  
C.A. Ferguson ◽  
Z. Hardcastle ◽  
...  
Keyword(s):  
Neural Crest ◽  
Homeobox Gene ◽  
Branchial Arch ◽  
Cranial Neural Crest ◽  
Loss Of Function ◽  
Molecular Events ◽  
Maxillary Molar ◽  
Molar Teeth ◽  
Cranial Neural Crest Cells ◽  
Arch Neural

The molecular events of odontogenic induction are beginning to be elucidated, but until now nothing was known about the molecular basis of the patterning of the dentition. A role for Dlx-1 and Dlx-2 genes in patterning of the dentition has been proposed with the genes envisaged as participating in an ‘odontogenic homeobox gene code’ by specifying molar development. This proposal was based on the restricted expression of the genes in molar ectomesenchyme derived from cranial neural crest cells prior to tooth initiation. Mice with targeted null mutations of both Dlx-1 and Dlx-2 homeobox genes do not develop maxillary molar teeth but incisors and mandibular molars are normal. We have carried out heterologous recombinations between mutant and wild-type maxillary epithelium and mesenchyme and show that the ectomesenchyme underlying the maxillary molar epithelium has lost its odontogenic potential. Using molecular markers of branchial arch neural crest (Barx1) and commitment to chondrogenic differentiation (Sox9), we show that this population alters its fate from odontogenic to become chondrogenic. These results provide evidence that a subpopulation of cranial neural crest is specified as odontogenic by Dlx-1 and Dlx-2 genes. Loss of function of these genes results in reprogramming of this population of ectomesenchyme cells into chondrocytes. This is the first indication that the development of different shaped teeth at different positions in the jaws is determined by independent genetic pathways.

scholarly journals Neural Crest Development and Craniofacial Morphogenesis Is Coordinated by Nitric Oxide and Histone Acetylation

2014 ◽  
Vol 21 (4) ◽  
pp. 488-501 ◽  
Author(s):  
Yawei Kong ◽  
Michael Grimaldi ◽  
Eugene Curtin ◽  
Max Dougherty ◽  
Charles Kaufman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Neural Crest ◽  
Histone Acetylation ◽  
Neural Crest Development ◽  
Craniofacial Morphogenesis

scholarly journals Specific inactivation of Twist1 in the mandibular arch neural crest cells affects the development of the ramus and reveals interactions with hand2

2012 ◽  
Vol 241 (5) ◽  
pp. 924-940 ◽  
Author(s):  
Yanping Zhang ◽  
Evan L. Blackwell ◽  
Mitchell T. McKnight ◽  
Gregory R. Knutsen ◽  
Wendy T. Vu ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Mandibular Arch ◽  
Arch Neural

Synergy betweenHoxa1andHoxb1: the relationship between arch patterning and the generation of cranial neural crest

Development ◽  
2001 ◽  
Vol 128 (15) ◽  
pp. 3017-3027 ◽  
Author(s):  
Anthony Gavalas ◽  
Paul Trainor ◽  
Linda Ariza-McNaughton ◽  
Robb Krumlauf
Keyword(s):  
Neural Crest ◽  
Double Mutant ◽  
Hox Genes ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Vital Role ◽  
Cranial Neural Crest ◽  
Double Mutation ◽  
Signalling Molecules ◽  
Arch Neural

Hoxa1 and Hoxb1 have overlapping synergistic roles in patterning the hindbrain and cranial neural crest cells. The combination of an ectoderm-specific regulatory mutation in the Hoxb1 locus and the Hoxa1 mutant genetic background results in an ectoderm-specific double mutation, leaving the other germ layers impaired only in Hoxa1 function. This has allowed us to examine neural crest and arch patterning defects that originate exclusively from the neuroepithelium as a result of the simultaneous loss of Hoxa1 and Hoxb1 in this tissue. Using molecular and lineage analysis in this double mutant background we demonstrate that presumptive rhombomere 4, the major site of origin of the second pharyngeal arch neural crest, is reduced in size and has lost the ability to generate neural crest cells. Grafting experiments using wild-type cells in cultured normal or double mutant mouse embryos demonstrate that this is a cell-autonomous defect, suggesting that the formation or generation of cranial neural crest has been uncoupled from segmental identity in these mutants. Furthermore, we show that loss of the second arch neural crest population does not have any adverse consequences on early patterning of the second arch. Signalling molecules are expressed correctly and pharyngeal pouch and epibranchial placode formation are unaffected. There are no signs of excessive cell death or loss of proliferation in the epithelium of the second arch, suggesting that the neural crest cells are not the source of any indispensable mitogenic or survival signals. These results illustrate that Hox genes are not only necessary for proper axial specification of the neural crest but that they also play a vital role in the generation of this population itself. Furthermore, they demonstrate that early patterning of the separate components of the pharyngeal arches can proceed independently of neural crest cell migration.

scholarly journals Actin capping protein CAPZB regulates cell morphology, differentiation, and neural crest migration in craniofacial morphogenesis

2016 ◽  
Vol 25 (7) ◽  
pp. 1255-1270 ◽  
Author(s):  
Kusumika Mukherjee ◽  
Kana Ishii ◽  
Vamsee Pillalamarri ◽  
Tammy Kammin ◽  
Joan F. Atkin ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Morphology ◽  
Capping Protein ◽  
Actin Capping Protein ◽  
Actin Capping ◽  
Neural Crest Migration ◽  
Craniofacial Morphogenesis

Homeotic transformation of branchial arch identity after Hoxa2 overexpression

Development ◽  
2000 ◽  
Vol 127 (24) ◽  
pp. 5355-5365 ◽  
Author(s):  
G.A. Grammatopoulos ◽  
E. Bell ◽  
L. Toole ◽  
A. Lumsden ◽  
A.S. Tucker
Keyword(s):  
Neural Crest ◽  
Branchial Arch ◽  
Reverse Transformation ◽  
Surrounding Tissue ◽  
Homeotic Transformation ◽  
Branchial Arches ◽  
Arch Neural

Overexpression of Hoxa2 in the chick first branchial arch leads to a transformation of first arch cartilages, such as Meckel's and the quadrate, into second arch elements, such as the tongue skeleton. These duplicated elements are fused to the original in a similar manner to that seen in the Hoxa2 knockout, where the reverse transformation of second to first arch morphology is observed. This confirms the role of Hoxa2 as a selector gene specifying second arch fate. When first arch neural crest alone is targeted, first arch elements are lost, but the Hoxa2-expressing crest is unable to develop into second arch elements. This is not due to Hoxa2 preventing differentiation of cartilages. Upregulation of a second arch marker in the first arch, and homeotic transformation of cartilage elements is only produced after global Hoxa2 overexpression in the crest and the surrounding tissue. Thus, although the neural crest appears to contain some patterning information, it needs to read cues from the environment to form a coordinated pattern. Hoxa2 appears to exert its effect during differentiation of the cartilage elements in the branchial arches, rather than during crest migration, implying that pattern is determined quite late in development.

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