Gap junctions - channels between cells that are made of connexins - play important roles in development. Connexin 43 (Cx43α1)knockout mice, for example, die soon after birth because of a heart defect. They also lack germ cells, and on , Francis and Lo report that this second defect is caused by increased apoptosis of primordial germ cells (PGCs). Using an Oct4-GFP transgene to track PGCs in mouse embryos, the researchers found no difference in PGC distribution or abundance between wild-type and Cx43α hetero- or homozygous knockout embryos during early development. Thus, PGCs are specified and migrate normally in the absence of connexin 43. However, at embryonic day 11.5, Cx43α knockout mice had fewer PGCs because of their increased apoptosis. This was associated with abnormal p53 activation and reduced β1-integrin function in the PGCs; inhibition of p53 activation rescued PGC cell death. Francis and Lo conclude that anoikis - apoptosis triggered by the disruption of extracellular matrix binding - is partly responsible for the germ-cell deficiency of Cx43α knockout mice.
