Primordial germ cells (PGCs) are the founder cells of the gametes. In the mouse, they can first be identified at embryonic day (E) 7 in the extraembryonic mesoderm, posterior to the primitive streak. By E8, PGCs are being incorporated into the hindgut epithelium. Between E9.5 and E11.5, the PGCs migrate through the dorsal mesentery to the genital ridges on the dorsal abdominal wall. PGCs leave the hindgut independently, but then extend long filopodial processes which connect neighboring PGCs to each other. As they arrive at the genital ridge, PGCs aggregate and then combine with somatic cells to form the gonad. The receptors governing these cell-cell interactions have not been characterized. We therefore examined E-cadherin as a candidate molecule due to its widespread role in cell-cell adhesion during embryogenesis, and because of the observation that PGC aggregation can be disrupted by incubation in calcium free media. Embryos were dissected from FVB mice on F9.5-E14.5 of timed pregnancies. Wholemount immunohistochemistry and confocal microscopy were performed with monoclonal antibodies against E-cadherin and SSEA-1, a PGC-specific marker. As PGCs leave the hindgut at E9.5, they are negative for E-cadherin. Expression is first seen at E10, when the PGCs are migrating through the dorsal mesentery. This staining is concentrated at sites of cell-cell contact. E-cadherin continues to be expressed through E14.5 in both male and female germ cells. These results indicate that E-cadherin may play important roles in PGC aggregation and in turning off migration. It does not, however, appear to be required in the incorporation of PGCs into the hindgut.