Related Experiment Video

Updated: Sep 21, 2026

Xenopus laevis as a Model to Identify Translation Impairment
10:24

Xenopus laevis as a Model to Identify Translation Impairment

Published on: September 27, 2015

Mitogen-activated protein kinase regulates normal transition from metaphase to interphase following parthenogenetic

H Tatemoto1, N Muto

  • 1School of Bioresources, Hiroshima Prefectural University, Shobara, Japan. hidettmt@bio.hiroshima-pu.ac.jp

Zygote (Cambridge, England)
|March 29, 2001
PubMed

Insights

Delayed mitogen-activated protein kinase (MAPK) inactivation is crucial for the second polar body emission in porcine oocytes. This finding clarifies the role of MAPK in the transition from meiosis to mitosis after egg activation.

Area of Science:

  • Cell Biology
  • Reproductive Biology
  • Molecular Biology

Background:

  • Maturation-promoting factor (MPF) and mitogen-activated protein kinase (MAPK) activities decrease after egg activation, but the precise function of delayed MAPK inactivation remains unclear.
  • Understanding the role of MAPK is essential for comprehending the transition from metaphase to interphase in oocyte maturation.

Purpose of the Study:

  • To investigate the essential role of MAPK activity in supporting the metaphase-to-interphase transition in in vitro matured porcine oocytes.
  • To elucidate the specific functions of delayed MAPK inactivation following egg activation.

Main Methods:

  • Porcine oocytes matured in vitro were arrested at metaphase II (MII).
  • MAPK activity was inhibited using U0126, a specific MAPK kinase inhibitor.
  • Artificial activation was induced via electrostimulation, with or without U0126 treatment, to analyze MAPK and histone H1 kinase (H1K) inactivation dynamics.

Main Results:

  • Inhibition of MAPK with U0126 in MII-arrested oocytes led to pronucleus (PN) formation but inhibited second polar body (PB-2) emission.
  • Electrostimulation induced inactivation of both H1K and MAPK, with H1K inactivation preceding MAPK.
  • U0126 treatment significantly accelerated MAPK inactivation and markedly inhibited PB-2 emission, while PN formation remained largely unaffected.

Conclusions:

  • Decreased MAPK activity is partly involved in driving oocytes from metaphase to interphase, facilitating PN development.
  • Delayed MAPK inactivation after MPF inactivation plays a critical role in PB-2 emission, essential for the transition from meiosis to mitosis.

More Related Videos

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development09:32

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Published on: June 15, 2017

Proteolytically Degraded Alginate Hydrogels and Hydrophobic Microbioreactors for Porcine Oocyte Encapsulation07:45

Proteolytically Degraded Alginate Hydrogels and Hydrophobic Microbioreactors for Porcine Oocyte Encapsulation

Published on: July 30, 2020

Related Concept Videos

Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...