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Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry
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Hypomorphic mutation in an essential cell-cycle kinase causes growth retardation and impaired spermatogenesis

Jung Min Kim1, Naofumi Takemoto, Ken-ichi Arai

  • 1Department of Cell Biology, Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo 113-8613, Japan.

The EMBO Journal
|October 1, 2003
PubMed

Insights

Cell division cycle 7 (Cdc7) kinase is crucial for DNA replication. Insufficient Cdc7 protein causes growth retardation and developmental issues in mice, highlighting its essential role in cell cycle regulation and mammalian meiosis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Developmental Biology

Background:

  • Cdc7 kinase is vital for initiating DNA replication.
  • Cdc7 knockout mouse embryonic stem cells are non-viable but can be rescued by a transgene.
  • Cdc7(-/-)tg ES cells exhibit normal growth, but the corresponding mice show growth retardation.

Purpose of the Study:

  • To investigate the role of Cdc7 protein levels in mouse development.
  • To understand the impact of Cdc7 insufficiency on cell cycle progression and meiosis.
  • To determine the critical threshold of Cdc7 for normal mammalian development.

Main Methods:

  • Generation of Cdc7(-/-)tg mice and embryonic fibroblasts (MEFs).
  • Analysis of cell cycle progression (S phase entry and progression) in MEFs.
  • Assessment of spermatogenesis in Cdc7(-/-)tg mice.
  • Correlation of Cdc7 protein levels with developmental phenotypes.

Main Results:

  • Cdc7(-/-)tg MEFs show delayed S phase entry and slow progression.
  • Spermatogenesis in Cdc7(-/-)tg mice is disrupted before meiotic prophase I.
  • Low Cdc7 protein levels in testes correlate with impaired spermatogenesis.
  • Increased Cdc7 expression via an additional transgene allele rescues growth and developmental defects.

Conclusions:

  • A critical level of the cell-cycle regulator Cdc7 is required for normal mouse development.
  • Cdc7 plays essential roles in mammalian meiotic processes.
  • Developmental abnormalities in Cdc7(-/-)tg mice are attributed to Cdc7 protein insufficiency.

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