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First published online August 14, 2006

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PGCs mind the gap

Gap junctions - channels between cells that are made of connexins - play important roles in development. Connexin 43 (Cx431) 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.

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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]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?