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Deficiency of TBL1XR1 causes asthenozoospermia
Author(s) -
Zhou Qiao,
Xu Miaofei,
Wang Xin,
Yu Mingming,
Chen Xiaojiao,
Lu Jing,
Zhou Ran,
Zhang Junqiang,
Ling Xiufeng,
Ji Juan
Publication year - 2021
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13980
Subject(s) - asthenozoospermia , motility , biology , sperm motility , small interfering rna , chromatin immunoprecipitation , sperm , microbiology and biotechnology , gene , male infertility , rna , genetics , gene expression , infertility , promoter , pregnancy
Transducin (β)‐like 1 X‐linked receptor 1 (TBL1XR1) is an evolutionarily conserved protein related to spermatozoa. To clarify its role and mechanism of action in spermatozoa, qRT‐PCR was used to analyse the expression of TBL1XR1 in human spermatozoa and mouse testes. The mice were established as an animal model by injecting the mice testes with small interfering RNA against TBL1XR1 or control siRNA. Our results indicated that deficiency of TBL1XR1 in mice reduced the motility of spermatozoa and disrupted the histone‐to‐protamine transition. We also found the decreased expression of TBL1XR1 in the spermatozoa of human patients with asthenozoospermia (AZ) compared with that in the spermatozoa of healthy males. Moreover, we carried out chromatin immunoprecipitation analyses and found that genes downstream of TBL1XR1 were related to sperm motility. Thus, TBL1XR1 might be related to sperm motility and might function through its downstream genes. Our data highlight the role of TBL1XR1 involved in spermatozoa and provide new molecular insights into the intricate systems required for male fertility.