Open AccessEmi2 Is Essential for Mouse Spermatogenesis
Author(s) -
Lakshmi Gopinathan,
Radosław Szmyd,
Diana Low,
M. Kasim Diril,
HengYu Chang,
Vincenzo Coppola,
Kui Liu,
Lino Tessarollo,
Ernesto Guccione,
Ans M. M. van Pelt,
Philipp Kaldis
Publication year - 2017
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2017.06.033
Subject(s) - meiosis , biology , knockout mouse , prophase , spermatogenesis , microbiology and biotechnology , mitosis , cyclin dependent kinase 1 , metaphase , embryonic stem cell , cell cycle checkpoint , homologous chromosome , cell cycle , genetics , cell , chromosome , endocrinology , gene
The meiotic functions of Emi2, an inhibitor of the APC/C complex, have been best characterized in oocytes where it mediates metaphase II arrest as a component of the cytostatic factor. We generated knockout mice to determine the in vivo functions of Emi2-in particular, its functions in the testis, where Emi2 is expressed at high levels. Male and female Emi2 knockout mice are viable but sterile, indicating that Emi2 is essential for meiosis but dispensable for embryonic development and mitotic cell divisions. We found that, besides regulating cell-cycle arrest in mouse eggs, Emi2 is essential for meiosis I progression in spermatocytes. In the absence of Emi2, spermatocytes arrest in early diplotene of prophase I. This arrest is associated with decreased Cdk1 activity and was partially rescued by a knockin mouse model of elevated Cdk1 activity. Additionally, we detected expression of Emi2 in spermatids and sperm, suggesting potential post-meiotic functions for Emi2.
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