Fig. 3: Deletion of mouse CCER1 results in male sterility.
From: Phase-separated CCER1 coordinates the histone-to-protamine transition and male fertility
a Body size of Ccer1+/+ and CRISPR/Cas9-editing used to generate Ccer1−/− mice. b Protein validation of Ccer1+/+ and CRISPR/Cas9-mediated deletion of CCER1 and the testis and epididymal morphology in Ccer1−/− mice. The samples derive from the same experiment and that blots were processed in parallel. c Breeding experiments with Ccer1−/−, Ccer1+/− and Ccer1+/+ males. Mice of each genotype (−58 bp, −29 bp, −8 bp) were crossed with fertile mates. The results (the mean ± SD) were determined using males in cages housing all three Ccer1−/− lines (Homozygous of Nwildtype = 24, N−58bp = 20, N−29bp = 2, N−8bp = 2; and Heterozygous of N−58bp = 21). d PNA staining revealed the morphology associated with the 16-step spermatid development process in the Ccer1−/− testes and Ccer1+/+ testes; the results show round-to-elongated spermatids with abnormal sperm heads. Scale bar: 10 μm. e Histologically determined morphology of the seminiferous epithelial tissue in the mouse testis revealed a spermiation failure in stage IX (arrow). Scale bar: 20 μm. f In addition, compared to those in the Ccer1+/+ mice, the spermatozoa in the epididymis of Ccer1−/− mice presented a larger number of malformations. Scale bar: 10 μm. g Statistical comparison of the number of abnormal spermatozoa between Ccer1−/− and Ccer1+/+ mice (8.70% ± 1.24% and 64.60% ± 7.57%, n = 3 for each genotype biological independent mice), Two-sided student’s t-test. Error bars, mean ± SD. P = 6.01 × 10−3. Source data are provided as a Source Data file.
