Slc26a1 is not essential for spermatogenesis and male fertility in mice

Author:

Meng Zhixiang1,Qiao Yu2,Xue Jiajia1,Wu Tiantian3,Gao Wenxin3,Huang Xiaoyan3,Lv Jinxing1,Liu Mingxi4,Shen Cong5

Affiliation:

1. Dushu Lake Hospital Affiliated to Soochow University, Center for Reproduction, Suzhou Dushu Lake Hospital, Suzhou, Jiangsu, China

2. The Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University, Center for Reproduction, Huai’an, Jiang Su, China

3. Department of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, State Key Laboratory of Reproductive Medicine, Nanjing, Jiangsu, China

4. 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

5. 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

Abstract

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.

Funder

National Key Research and Development Program of China

University Synergy Innovation Program of Anhui Province

Suzhou Science and Technology Development Plan

Clinical Medicine Experts of Suzhou Industrial Park

Publisher

PeerJ

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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