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Emi2 Is Essential for Mouse Spermatogenesis

Gopinathan, Lakshmi ; Szmyd, Radoslaw ; Low, Diana ; Diril, M. Kasim ; Chang, Heng Yu ; Coppola, Vincenzo ; Liu, Kui ; Tessarollo, Lino ; Guccione, Ernesto and van Pelt, Ans M.M. , et al. (2017) In Cell Reports 20(3). p.697-708
Abstract

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... (More)

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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publishing date
type
Contribution to journal
publication status
published
subject
keywords
APC/C, Cdk1, diplotene, Emi2, knockout mice, meiosis, ovary, phosphorylation, spermatocytes, spermatogenesis
in
Cell Reports
volume
20
issue
3
pages
12 pages
publisher
Cell Press
external identifiers
  • pmid:28723571
  • scopus:85025091691
ISSN
2211-1247
DOI
10.1016/j.celrep.2017.06.033
language
English
LU publication?
no
id
b294e723-ae17-4d5a-9f95-ad70a13ab0e6
date added to LUP
2019-09-18 10:12:05
date last changed
2020-10-27 01:17:34
@article{b294e723-ae17-4d5a-9f95-ad70a13ab0e6,
  abstract     = {<p>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.</p>},
  author       = {Gopinathan, Lakshmi and Szmyd, Radoslaw and Low, Diana and Diril, M. Kasim and Chang, Heng Yu and Coppola, Vincenzo and Liu, Kui and Tessarollo, Lino and Guccione, Ernesto and van Pelt, Ans M.M. and Kaldis, Philipp},
  issn         = {2211-1247},
  language     = {eng},
  month        = {07},
  number       = {3},
  pages        = {697--708},
  publisher    = {Cell Press},
  series       = {Cell Reports},
  title        = {Emi2 Is Essential for Mouse Spermatogenesis},
  url          = {http://dx.doi.org/10.1016/j.celrep.2017.06.033},
  doi          = {10.1016/j.celrep.2017.06.033},
  volume       = {20},
  year         = {2017},
}