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Published on: March 14, 2017
Parathyroid hormone-related peptide (PTHrP) induces parietal endoderm formation exclusively via the type I PTH/PTHrP
M H Verheijen1, M Karperien, U Chung
1Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Insights
Parathyroid hormone-related protein (PTHrP) and its type I receptor are crucial for parietal endoderm (PE) differentiation in mouse embryos. While not essential for initial PE formation, they are required for proper PE development and function.
Area of Science:
- Developmental Biology
- Endocrinology
- Molecular Biology
Background:
- The parathyroid hormone-related protein (PTHrP) and its type I receptor are implicated in early mouse embryogenesis, specifically in parietal endoderm (PE) formation.
- Previous studies indicated normal PE formation but smaller size and embryonic lethality in type I receptor knockout embryos.
Purpose of the Study:
- To investigate the precise role of PTHrP and its type I receptor in mouse parietal endoderm differentiation and embryonic development.
- To elucidate the interaction between PTHrP and the type I receptor during early embryogenesis.
Main Methods:
- Utilized novel antibodies to detect type I receptor and PTHrP protein expression in mouse embryos.
- Performed homologous recombination in embryonic stem (ES) cells to delete the type I PTH/PTHrP receptor.
- Assessed PE formation and differentiation in wild-type and knockout embryos.
Main Results:
- A growth defect in type I receptor knockout embryos was observed as early as day 8.5 post-coitum (p.c.).
- Type I receptor protein expression was localized to extraembryonic endoderm, while PTHrP was found in adjacent trophoblast giant cells, suggesting paracrine signaling.
- Complete prevention of PTHrP-induced PE differentiation occurred upon deletion of the type I receptor in ES cells.
Conclusions:
- PTHrP and the type I PTH/PTHrP receptor are essential for the proper differentiation and/or functioning of parietal endoderm.
- These molecules are not required for the initial formation of PE but play a critical role in its subsequent development.
Abstract:
A number of studies suggest a role for PTHrP and the classical PTH/PTHrP receptor (type I) in one of the first differentiation processes in mouse embryogenesis, i.e. the formation of parietal endoderm (PE). We previously reported that although in type I receptor (-/-) embryos PE formation seemed normal, the embryos were smaller from at least day 9.5 p.c. and 60% had died before day 12.5 p.c. Here we show that the observed growth defect commences even earlier, at day 8.5 p.c. Using two novel antibodies, we show that the expression of the type I receptor protein at this stage is confined to extraembryonic endoderm only. In addition, we show that large amounts of PTHrP protein are present in the adjacent trophoblast giant cells, suggesting a paracrine interaction of PTHrP and the type I PTH/PTHrP receptor in PE formation. The involvement in PE differentiation of other recently described receptors for PTHrP would explain a possible redundancy for the type I receptor in PE formation. However, deletion of the type I PTH/PTHrP receptor in ES cells by homologous recombination completely prevents PTHrP-induced PE differentiation. Based upon these observations, we propose that PTHrP and the type I PTH/PTHrP receptor, although not required for the initial formation of PE, are required for its proper differentiation and/or functioning.
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