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Meiosis II

Meiosis II

Meiosis II entails cell division and segregation of the sister chromatids, resulting in the production of four unique haploid gametes. The steps for meiosis II are similar to mitosis, except that meiosis II occurs in haploid cells, whereas mitosis occurs in diploid cells.
The timing and cell division patterns of meiosis differ between males and females. In male meiosis, the centrosomes are part of the formation of the meiotic spindle. However, in oocytes, including that of humans, Drosophila,...

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Multi-Photon Laser Ablation of Cytoplasmic Microtubule Organizing Centers in Mouse Oocytes

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Published on: November 11, 2022

Cyclin E ablation in the mouse.

Yan Geng¹, Qunyan Yu, Ewa Sicinska

¹Department of Cancer Biology, Dana-Farber Cancer Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.

|August 28, 2003

Summary

This summary is machine-generated.

E type cyclins are largely dispensable for mouse development but essential for cell cycle reentry. Lacking cyclin E impairs DNA replication origin licensing and reduces oncogenic transformation resistance.

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Area of Science:

Cell Biology
Molecular Biology
Developmental Biology

Background:

E type cyclins (E1 and E2) are generally thought to regulate entry into S phase and are considered essential for all cell proliferation.
The precise roles and necessity of cyclin E in different cell types and developmental processes remain incompletely understood.

Purpose of the Study:

To investigate the role of E type cyclins in mouse development and cell cycle regulation.
To elucidate the molecular mechanisms underlying the function of cyclin E in cell proliferation and transformation.

Main Methods:

Generation of cyclin E-deficient mice.
Analysis of cell proliferation, cell cycle progression, and DNA replication in various cell types.
Molecular analysis of MCM protein loading onto replication origins.
Assessment of oncogenic transformation potential in cyclin E-deficient cells.

Main Results:

E type cyclins are not essential for overall mouse development but are crucial for endoreplication in trophoblast giant cells and megakaryocytes.
Cyclin E-deficient cells can proliferate continuously but fail to reenter the cell cycle from quiescence (G0 state).
Absence of cyclin E leads to impaired MCM protein incorporation into DNA replication origins during G0 to S phase transition.
Cyclin E-deficient cells exhibit resistance to oncogenic transformation.

Conclusions:

E type cyclins play a critical role in enabling cell cycle reentry from quiescence.
The function of cyclin E in DNA replication origin licensing is vital for specific cell types and processes.
Cyclin E has a differential impact on normal proliferation versus oncogenic transformation, suggesting distinct regulatory pathways.