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Reduced spermatogonial proliferation and decreased fertility in mice overexpressing cyclin e in spermatogonia

Academic Article
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Overview

authors

  • Liberal, V.
  • De Miguel, M. P.
  • Henze, M.
  • Nistal, M.
  • Reed, Steven

publication date

  • October 2010

journal

  • Cell Cycle  Journal

abstract

  • Cyclin E is a key component of the cell cycle regulatory machinery, contributing to the activation of Cdk2 and the control of cell cycle progression at several stages. Cyclin E expression is tightly regulated, by periodic transcription and ubiquitin-mediated degradation. Overexpression of cyclin E has been associated with tumor development and poor prognosis in several tumor types, including germ cell tumors and both cyclin E and its partner Cdk2 are required for normal spermatogenesis. Here we have generated and characterized transgenic mice overexpressing a cyclin E mutant protein, resistant to ubiquitin-mediated proteolysis, in testicular germ cells, under the control of the human EF-1alpha promoter. The transgenic mice develop normally and live a normal life span, with no signs of testicular tumor development. The transgenic mice display however reduced fertility and testicular atrophy, due to reduced spermatogonial proliferation as a consequence of deregulated cyclin E levels. Overall our results show that deregulation of cyclin E expression contribute to infertility, due to inability of the spermatogonial cells to start the mitotic cycles prior to entering meiosis.

subject areas

  • Animals
  • Cell Cycle
  • Cell Proliferation
  • Cyclin E
  • Female
  • Fertility
  • HEK293 Cells
  • Humans
  • Male
  • Mice
  • Mice, Transgenic
  • Spermatogenesis
  • Spermatogonia
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Research

keywords

  • cyclin E overexpression
  • fertility
  • spermatogonia
  • testis
  • transgenic mouse
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Identity

PubMed Central ID

  • PMC3055205

International Standard Serial Number (ISSN)

  • 1538-4101

Digital Object Identifier (DOI)

  • 10.4161/cc.9.20.13544

PubMed ID

  • 20962587
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Additional Document Info

start page

  • 4222

end page

  • 4227

volume

  • 9

issue

  • 20

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