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Overexpression of ubiquitin carboxyl‐terminal hydrolase L1 arrests spermatogenesis in transgenic mice
Author(s) -
Wang YuLai,
Liu Wanzhao,
Sun YingJie,
Kwon Jungkee,
Setsuie Rieko,
Osaka Hitoshi,
Noda Mami,
Aoki Shunsuke,
Yoshikawa Yasuhiro,
Wada Keiji
Publication year - 2006
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20364
Subject(s) - biology , spermatogenesis , proliferating cell nuclear antigen , sertoli cell , downregulation and upregulation , germ cell , somatic cell , apoptosis , spermatocyte , transgene , genetically modified mouse , microbiology and biotechnology , meiosis , ubiquitin , cell growth , endocrinology , genetics , gene
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. Mol. Reprod. Dev. © 2005 Wiley‐Liss, Inc.