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Characterization of the fate of midline epithelial cells during the fusion of mandibular prominences in vivo
Author(s) -
Chai Yang,
Sasano Yasuyuki,
Bringas Pablo,
Mayo Mark,
Kaartinen Vesa,
Heisterkamp Nora,
Groffen John,
Slavkin Harold,
Shuler Charles
Publication year - 1997
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/(sici)1097-0177(199704)208:4<526::aid-aja8>3.0.co;2-k
Subject(s) - mesenchyme , biology , cell fusion , epithelium , anatomy , programmed cell death , microbiology and biotechnology , apoptosis , cell , embryo , genetics
Abstract The fusion of the mandibular prominences along the midline is achieved with the absence of medial epithelial cells at the fusion site. Failure of fusion of the mandibular prominences results in median cleft of the lower lip and mandible. Cellular and molecular events controlling mandibular fusion were examined during the fusion process in mouse embryogenesis. Cell lineage analyses at the fusion site revealed that epithelial cells migrated to the surface and oral epithelia. DiI‐labeled epithelial cells were not observed within the mandibular mesenchyme at any stage of fusion. Examination of the midline region did not reveal cells with ultrastructural changes characteristic of apoptotic cell death. An increase in lysosomal enzymes in the midline epithelial cells, which would be correlated with programmed cell death, was not observed. Mice lacking TGF‐β3 did not have cleft mandible, but had clefting of the secondary palate as a feature of null mutation phenotype. We interpret our comparisons between wild type and homozygous TGF‐β3 (‐/‐) mice to suggest that different developmental processes control palatal vs. mandibular fusion. We hypothesize that medial epithelial cells at the fusion site of mandibular prominences migrate to the surface epithelium during the fusion process and neither transdifferentiate into mesenchyme nor express apoptosis. Dev. Dyn. 208:526–535, 1997. © 1997 Wiley‐Liss, Inc.