Neural crest and placode roles in formation and patterning of cranial sensory ganglia in lamprey

genesis ◽  
2020 ◽  
Vol 58 (5) ◽  
Author(s):  
Tian Yuan ◽  
Joshua R. York ◽  
David W. McCauley
Development ◽  
1999 ◽  
Vol 126 (22) ◽  
pp. 5011-5026 ◽  
Author(s):  
J.R. Barrow ◽  
M.R. Capecchi

The rhombencephalic neural crest play several roles in craniofacial development. They give rise to the cranial sensory ganglia and much of the craniofacial skeleton, and are vital for patterning of the craniofacial muscles. The loss of Hoxa1 or Hoxa2 function affects the development of multiple neural crest-derived structures. To understand how these two genes function together in craniofacial development, an allele was generated that disrupts both of these linked genes. Some of the craniofacial defects observed in the double mutants were additive combinations of those that exist in each of the single mutants, indicating that each gene functions independently in the formation of these structures. Other defects were found only in the double mutants demonstrating overlapping or synergistic functions. We also uncovered multiple defects in the attachments and trajectories of the extrinsic tongue and hyoid muscles in Hoxa2 mutants. Interestingly, the abnormal trajectory of two of these muscles, the styloglossus and the stylohyoideus, blocked the attachment of the hyoglossus to the greater horn of the hyoid, which in turn correlated exactly with the presence of cleft palate in Hoxa2 mutants. We suggest that the hyoglossus, whose function is to depress the lateral edges of the tongue, when unable to make its proper attachment to the greater horn of the hyoid, forces the tongue to adopt an abnormal posture which blocks closure of the palatal shelves. Unexpectedly, in Hoxa1/Hoxa2 double mutants, the penetrance of cleft palate is dramatically reduced. We show that two compensatory defects, associated with the loss of Hoxa1 function, restore normal attachment of the hyoglossus to the greater horn thereby allowing the palatal shelves to lift and fuse above the flattened tongue.


BioFactors ◽  
2004 ◽  
Vol 21 (1-4) ◽  
pp. 15-18 ◽  
Author(s):  
Ichiro Matsumoto ◽  
Shugo Nakamura ◽  
Yasufumi Emori ◽  
Soichi Arai ◽  
Keiko Abe

2014 ◽  
Vol 199 (4) ◽  
pp. 278-293 ◽  
Author(s):  
Mohammed Abu El-Magd ◽  
Ayman A. Saleh ◽  
Foad Farrag ◽  
Reda M. Abd El-Aziz ◽  
Haytham A. Ali ◽  
...  

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 421-433
Author(s):  
J.L. Duband ◽  
J.P. Thiery

Neural crest cells express different adhesion modes at each phase of their development starting with their separation from the neural tube, followed by migration along definite pathways throughout the embryo, and finally to settlement and differentiation in elected embryonic regions. In order to determine possible changes in the cytoskeleton organization and function during these processes, we have studied the in situ distribution of two major cytoskeleton-associated elements involved in the membrane anchorage of actin microfilaments, i.e. vinculin and talin, during the ontogeny of the neural crest and its derivatives in the avian embryo. Prior to emigration, neural crest cells exhibited both vinculin and talin at levels similar to the neighbouring neural epithelial cells, and this expression apparently did not change as cells became endowed with migratory properties. However, vinculin became selectively enhanced in neural crest cells as they further migrated towards their final destination. This increase in vinculin amount was particularly striking in vagal and truncal neural crest cells entering cellular environments, such as the sclerotome and the gut mesenchyme. Talin was also expressed by neural crest cells but, in contrast to vinculin, staining was not conspicuous compared to neighbouring mesenchymal cells. High levels of vinculin persisted throughout embryogenesis in almost all neural derivatives of the neural crest, including the autonomous and sensory ganglia and Schwann cells along the peripheral nerves. In contrast, the non-neural derivatives of the neural crest rapidly lost their prominent vinculin staining after migration. The pattern of talin in the progeny of the neural crest was complex and varied with the cell types: for example, some cranial sensory ganglia expressed high amounts of the molecule whereas autonomic ganglia were nearly devoid of it. Our results suggest that (i) vinculin and talin may follow independent regulatory patterns within the same cell population, (ii) the level of expression of vinculin and talin in neural crest cells may be consistent with the rapid, constant modulations of their adhesive properties, and (iii) the expression patterns of the two molecules may also be correlated with the genesis of the peripheral nervous system.


2004 ◽  
Vol 126 (1) ◽  
pp. 98-102 ◽  
Author(s):  
Ichiro Matsumoto ◽  
Nami Nagamatsu ◽  
Soichi Arai ◽  
Yasufumi Emori ◽  
Keiko Abe

2002 ◽  
Vol 251 (1) ◽  
pp. 45-58 ◽  
Author(s):  
Peter Andermann ◽  
Josette Ungos ◽  
David W. Raible

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