Overexpression of ubiquitin carboxyl-terminal hydrolase L1 arrests spermatogenesis in transgenic mice

Yu Lai Wang, Wanzhao Liu, Ying Jie Sun, Jungkee Kwon, Rieko Setsuie, Hitoshi Osaka, Mami Noda, Shunsuke Aoki, Yasuhiro Yoshikawa, Keiji Wada

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69 Citations (Scopus)


Ubiquitin carboxyl-terminal hydrolase 1 (UCH-L1) can be detected in mouse testicular germ cells, mainly spermatogonia and somatic Sertoli cells, but its physiological role is unknown. We show that transgenic (Tg) mice overexpressing EF1α promoter-driven UCH-L1 in the testis are sterile due to a block during spermatogenesis at an early stage (pachytene) of meiosis. interestingly, almost all spermatogonia and Sertoli cells expressing excess UCH-L1, but little PCNA (proliferating cell nuclear antigen), showed no morphological signs of apoptosis or TUNEL-positive staining. Rather, germ cell apoptosis was mainly detected in primary spermatocytes having weak or negative UCH-L1 expression but strong PCNA expression. These data suggest that overexpression of UCH-L1 affects spermatogenesis during meiosis and, in particular, induces apoptosis in primary spermatocytes. In addition to results of caspases-3 upregulation and Bcl-2 downregulation, excess UCH-L1 influenced the distribution of PCNA, suggesting a specific role for UCH-L1 in the processes of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis.

Original languageEnglish
Pages (from-to)40-49
Number of pages10
JournalMolecular Reproduction and Development
Issue number1
Publication statusPublished - Jan 2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Genetics
  • Developmental Biology
  • Cell Biology


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