The role of Connexin31.1 for mouse trophoblast cell lineage development and function of placental glycogen cells

• Antragsteller: Dr. Mark Kibschull
• Fachliche Zuordnung: Zellbiologie
• Förderung: Förderung von 2006 bis 2008
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 20537615

The overall objective of this project is to define the role of gap junctional communication in mouse trophoblast differentiation and to distinguish the specific functions of connexin31.1 from connexin31. Null mutations of the Cx31 or the Cx31.1 gene in mice results in a transient placental dysfunction, which leads to embryonic death at midgestation. Both connexins are co-expressed in the trophectoderm of the blastocyst, and the early trophoblast cell lineage developing from this tissue. This implicates overlapping functions for both connexins during this developmental period, which will be proven by generating Cx31/Cx31.1 double knockout mice through molecular ES cell targeting. With formation of the chorioallantoic placenta after day 8.5 pc the expression of Cx31 and Cx31.1 separates into different compartments. Cx31 characterizes the diploid, proliferating trophoblast population of the chorionic plate and the spongiotrophoblast, whereas Cx31.1 is found only in the glycogen cells. In contrast to Cx31 knockout mice the lack of Cx31.1 does not lead to a clearly defined morphological phenotype of the placenta. Due to the specific expression in glycogen cells I hypothesize that the lack of Cx31.1 leads to embryonic death by: (1) impaired interstitial trophoblast invasion into the maternal decidua and/or (2) changed glycogen cell physiology causing placental dysfunction.

• DFG-Verfahren: Forschungsstipendien
• Internationaler Bezug: Kanada
• Gastgeber: Professor Dr. Stephen J. Lye