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Figure 7


Fig. 7. Analysis of ß1-integrin function in PGC motility. (A) Treatment of wild-type PGCs with a ß1-integrin-function-blocking antibody caused a significant reduction in both the speed and directionality of PGC migration in E11.5 genital ridge explants. The migration data was obtained from the analysis of 48 cells derived from five embryo explants for both sham and function-blocking antibody treatments. (B) PGC attachment to ß1-integrin-antibody-coated dishes was used to assess ß1-integrin-mediated cell adhesion. Homozygous Cx43{alpha}1KO PGCs showed a marked reduction in ß1-integrin-mediated adhesion, while control assays using plates coated with anti-mouse IgG antibodies showed no difference in adhesion between the different genotypes. It should be noted that the heterozygous KO PGCs also showed some reduction in adhesion to ß1-integrin-antibody-coated dishes, but less than that observed in the homozygous KO PGCs. For assessments of ß1-integrin-mediated adhesion, assays were carried out using PGCs derived from 14 Cx43{alpha}1 +/+, 20 Cx43{alpha}1 +/- and nine Cx43{alpha}1 -/- embryos, while control assays using anti-mouse IgG were carried out using PCGs from three Cx43{alpha}1 +/+, 14 Cx43{alpha}1 +/- and eight Cx43{alpha}1 -/- embryos.





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