Emi2 Is Essential for Mouse Spermatogenesis

Publication date: 18 July 2017
Source:Cell Reports, Volume 20, Issue 3
Author(s): Lakshmi Gopinathan, Radoslaw Szmyd, Diana Low, M. Kasim Diril, Heng-Yu Chang, Vincenzo Coppola, Kui Liu, Lino Tessarollo, Ernesto Guccione, Ans M.M. van Pelt, Philipp Kaldis
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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Teaser

Gopinathan et al. use mouse genetics to characterize the in vivo functions of Emi2, a meiotic inhibitor of APC/C. Emi2 knockout mice are sterile, revealing that Emi2 is essential for oocytes and spermatocytes to complete meiotic divisions. Impaired Cdk1 activity upon loss of Emi2 contributes to spermatogenic defects.


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