Abstract
© 1990 SAMiller
Cell proliferation measured with tritium autoradiograms shows a significant bilateral pattern that correlates with folding morphogenesis in chick and mouse endoderm. Lowest proliferation in median roof cells differs significantly from highest proliferation in adjacent walls that fold to enclose the tube. Active, localized changes in cell shape are lacking, but median endoderm cells are distinctly thin compared to cells in contiguous walls. These differentials suggest that the gut folds about the roof which effectively acts as a hinge. Apoptosis does not appear to be involved in early folding of chick endoderm. Lateral asymmetries are not apparent in chick endoderm, but 8.5 d.p.c. mice have significant right>left asymmetry in endoderm walls of open midgut. Notochord is proximate to early gut endoderm. Differences in the median domain persist after dorsal aortae spatially separate chick endoderm from notochord. The possibility that median endoderm is influenced by chordamesoderm in chick and mouse embryos needs further investigation. Folding endoderm to form gut tube appears to be a process that is driven by domains of high proportions of cell proliferation flanking a domain with significantly lower proliferative growth. This forces buckling of endoderm into lateral folds that eventually join and enclose a tube. The term, median hinge point (MHP) has been applied to neural epithelium, but this gut hinge is also a median hinge point in another epithelium. In the light of this new information, it may be more precise to refer to these hinge points as gut hinge point (GHP) and neural hinge point (NHP).
Supported by a Margaret Bundy Scott Fellowship, Sergei S. Zlinkoff Fund, Casstevens Family Fund, Sigma Xi, and Hamilton College and Kirkland College Research Grants. Includes data from Senior Thesis of AB, MC, TC, KJ and JT.
FASEB Journal 13: A346 (1999)
