First published online August 14, 2006
Development 133, 1704e (2006)
© The Company of Biologists Limited
PGCs mind the gap
Gap junctions - channels between cells that are made of connexins - play
important roles in development. Connexin 43 (Cx43
1)
knockout mice, for example, die soon after birth because of a heart defect.
They also lack germ cells, and on
p. 3451, 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 Cx43 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, Cx43 knockout mice had fewer PGCs because of their
increased apoptosis. This was associated with abnormal p53 activation and
reduced ß1-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 Cx43 knockout
mice.
Related articles in Development:
- Primordial germ cell deficiency in the connexin 43 knockout mouse arises from apoptosis associated with abnormal p53 activation
- Richard J. B. Francis and Cecilia W. Lo
Development 2006 133: 3451-3460.
[Abstract]
[Full Text]
