Disruption in ACTL7A causes acrosomal ultrastructural defects in human and mouse sperm as a novel male factor inducing early embryonic arrest

Author:

Xin Aijie12ORCID,Qu Ronggui1ORCID,Chen Guowu1ORCID,Zhang Ling134ORCID,Chen Junling1,Tao Chengqiu3,Fu Jing1,Tang Jianan2,Ru Yanfei2,Chen Ying1,Peng Xiandong1,Shi Huijuan2ORCID,Zhang Feng12345ORCID,Sun Xiaoxi146ORCID

Affiliation:

1. Shanghai Ji Ai Genetics and IVF Institute, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.

2. NHC Key Laboratory of Reproduction Regulation (Shanghai Institute of Planned Parenthood Research), School of Pharmacy, Fudan University, Shanghai, China.

3. State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.

4. Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, China.

5. State Key Laboratory of Reproductive Medicine, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.

6. Department of Endocrinology and Reproductive Medicine, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.

Abstract

ACTL7A deficiency is a novel male factor inducing early embryonic arrest that can be overcome by artificial oocyte activation.

Funder

National Natural Science Foundation of China

China Postdoctoral Science Foundation

Foundation of Science and Technology Commission of Shanghai Municipality

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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