Slc26a1 is not essential for spermatogenesis and male fertility in mice
Zhixiang Meng,
Yu Qiao,
Jiajia Xue,
Tiantian Wu,
Wenxin Gao,
Xiaoyan Huang,
Jinxing Lv,
Mingxi Liu,
Cong Shen
Affiliations
Zhixiang Meng
Dushu Lake Hospital Affiliated to Soochow University, Center for Reproduction, Suzhou Dushu Lake Hospital, Suzhou, Jiangsu, China
Yu Qiao
The Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University, Center for Reproduction, Huai’an, Jiang Su, China
Jiajia Xue
Dushu Lake Hospital Affiliated to Soochow University, Center for Reproduction, Suzhou Dushu Lake Hospital, Suzhou, Jiangsu, China
Tiantian Wu
Department of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, State Key Laboratory of Reproductive Medicine, Nanjing, Jiangsu, China
Wenxin Gao
Department of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, State Key Laboratory of Reproductive Medicine, Nanjing, Jiangsu, China
Xiaoyan Huang
Department of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, State Key Laboratory of Reproductive Medicine, Nanjing, Jiangsu, China
Jinxing Lv
Dushu Lake Hospital Affiliated to Soochow University, Center for Reproduction, Suzhou Dushu Lake Hospital, Suzhou, Jiangsu, China
Mingxi Liu
State Key Laboratory of Reproductive Medicine and Offspring Health, The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Jiangsu, China
Cong Shen
The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, State Key Laboratory of Reproductive Medicine, Center for Reproduction and Genetics, Suzhou Municipal Hospital, Suzhou, Jiangsu, China
Thousands of genes are expressed in the testis of mice. However, the details about their roles during spermatogenesis have not been well-clarified for most genes. The purpose of this study was to examine the effect of Slc26a1 deficiency on mouse spermatogenesis and male fertility. Slc26a1-knockout (KO) mice were generated using CRISPR/Cas9 technology on C57BL/6J background. We found no obvious differences between Slc26a1-KO and Slc26a1-WT mice in fertility tests, testicular weight, sperm concentrations, or morphology. Histological analysis found that Slc26a1-KO mouse testes had normal germ cell types and mature sperm. These findings indicated that Slc26a1 was dispensable for male fertility in mice. Our results may save time and resources by allowing other researchers to focus on genes that are more meaningful for fertility studies. We also found that mRNAs of two Slc26a family members (Slc26a5 and Slc26a11) were expressed on higher mean levels in Slc26a1-KO total mouse testes, compared to Slc26a1-WT mice. This effect was not found in mouse GC-1 and GC-2 germ cell lines with the Slc26a1 gene transiently knocked down. This result may indicate that a gene compensation phenomenon was present in the testes of Slc26a1-KO mice.
