To determine how the lens growth is affected by the Cx50-R205G mutation, we measured the mouse lens wet weight of different genotypes at ages from P3 to P42. The lens wet weight was recorded and plotted against the ages to generate the lens growth curve (
Fig. 2A). By calculating the average lens weight (n = 3–7 mice for each genotype at each time point) and performing the Student's
t-test, the homozygous Cx50(R205G/R205G) lenses showed the most severe reduction in the lens wet weight when compared with all other genotypes (
P < 0.001, compared with wild-type, at all time points;
P < 0.001, compared with heterozygous Cx50-R205G, at all time points except
P < 0.01 at P3) (
Fig. 2A), and the heterozygous Cx50(R205G/+) lenses had consistently lower lens weight, on average, than wild-type lenses at all postnatal timepoints (
P < 0.001 at all time points except
P < 0.01 at P7) (
Fig. 2A). Moreover, the average lens weight of homozygous Cx50(R205G/R205G) mice was consistently lower than that of the Cx50(–/–) knockout lenses (
P < 0.05 at P14 and
P < 0.001 at all other time points), indicating the distinct mechanism of lens growth disruption caused by the Cx50-R205G mutation and the deletion of Cx50 in the knockout mutant lenses (
Fig. 2A). Due to the lens rupture phenotype occurring in the homozygous Cx50(R205G/R205G) mice around weaning age, we were unable to obtain their lens wet weight beyond the age of 3 weeks. The disparity in lens wet weight between wild-type and Cx50 mutant lenses occurred early in development. At P3, while the average Cx50(–/–) lens mass was approximately 64% that of wild-type lenses (
P < 0.001), the average Cx50(R205G/R205G) lens mass was only approximately 46% that of the wild-type (
P < 0.001) (
Fig. 2B). At P7, the Cx50(–/–) knockout lens mass was approximately 60% that of wild-type (
P < 0.001), while the Cx50(R205G/R205G) lens was only approximately 35% of wild-type lens mass (
P < 0.001) (
Fig. 2B). At postnatal day 3, the heterozygous Cx50(R205G/+) lens mass was approximately 59% that of wild-type (
P < 0.001) and, at postnatal day 7, approximately 82% of wild-type (
P < 0.01). There was no significant difference in lens mass between heterozygous Cx50(R205G/+) and Cx50(–/–) knockout lenses at P3 (
P = 0.24); at P7, compared with the wild-type control, the Cx50(–/–) lens mass was reduced by approximately 40% (
P < 0.001) and the heterozygous Cx50(R205G/+) lens mass by approximately 18% (
P < 0.01) (
Fig. 2B), the Cx50(R205G/+) and Cx50(–/–) knockout lenses showed a significant difference between their lens mass (
P < 0.01), and the knockout lenses had a 25% mass reduction. Thus, the Cx50-R205G point mutation uniquely inhibits the neonatal lens growth.