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. 2011 Nov 18;6(11):e28039. doi: 10.1371/journal.pone.0028039

Figure 2. Post-meiotic germ cell-specific inactivation of β-catenin and associated reproductive defects.

Figure 2

(A) Schematic of the β-catenin-flox allele before (Ctnnb1F) and after (Ctnnb1FΔ) Prm1-cre-mediated recombination. β-catenin exons are numbered. F1, F2, R1, and R2 represent primers used for genotyping. (B) PCR genotype analyses of tail or testis genomic DNA using primers F1 and R1 or F2 and R2, respectively. Sequences and product sizes have been previously described [12]. (C) and (D) Prm1-cre hemizygous-β-catenin-flox homozygous (Ctnnb1 FΔ) male mice are severely sub-fertile. (C) Mean number of litters (n = 10, *p<0.05) and (D) mean number of pups per litter (n = 10, ***p<0.0001) obtained from eight-week timed matings of 6 to 8-week old Ctnnb1 FΔ mice and control littermates. (E) Ctnnb1 FΔ male mice exhibited significantly reduced testis to body weight ratio (n = 9, *p<0.05). (F) Ctnnb1 FΔ mice had significantly lower sonication-resistant spermatids count (n = 3, **p<0.01). (G) Caudal epididymal sperm count showed significantly fewer sperm in Ctnnb1 FΔ mice (n = 9, *p<0.05). (H) Significantly reduced number of caudal epididymal sperm with forward motility in Ctnnb1 FΔ mice (n = 9, *p<0.05).