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Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos
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AMPK Activity Contributes to G2 Arrest and DNA Damage Decrease via p53/p21 Pathways in Oxidatively Damaged Mouse

Pei He1,2,3, Zhiling Li1,2,3, Feng Xu4

  • 1Department of Reproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.

Frontiers in Cell and Developmental Biology
|October 5, 2020
PubMed
Summary
This summary is machine-generated.

Mild oxidative stress causes G2 arrest in mouse zygotes, involving AMPK activation. This pathway inhibits CDK1 via p53/p21, aiding DNA repair and embryo survival. Understanding this is key for viable embryo generation.

Keywords:
AMPKDNA damageG2 arrestin vitro fertilized embryosoxidative stressp21p53

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Area of Science:

  • Embryology
  • Cellular Biology
  • Molecular Biology

Background:

  • Zygotes possess DNA repair and G2/M checkpoint mechanisms that vary in response to stressors.
  • Mild oxidative stress in mouse zygotes causes a G2/M phase delay via spindle assembly checkpoint activation.
  • The role of G2 arrest and AMP-activated protein kinase (AMPK) in oxidative stress response in zygotes remains unclear.

Purpose of the Study:

  • To investigate if G2/M phase delay involves G2 arrest triggered by G2/M checkpoint activation.
  • To determine the involvement of AMPK in G2 arrest and DNA damage repair in mouse zygotes under oxidative stress.
  • To elucidate the molecular mechanisms of oxidative stress-induced embryonic developmental arrest.

Main Methods:

  • Mouse zygotes were treated with hydrogen peroxide (H2O2) to induce oxidative stress.
  • Detection of phosphorylated H2AX as a DNA damage marker.
  • Observation of AMPK phosphorylation, activation, and subcellular localization.
  • Inhibition of AMPK activity using Compound C and SBI-0206965.
  • Assessment of CDK1 activity, p53 and p21 protein levels, DNA damage, apoptosis, and embryo development rates.

Main Results:

  • Oxidative stress induced G2 arrest in mouse zygotes, with phosphorylated H2AX detected from early S phase.
  • AMPK was phosphorylated, activated, and translocated to the nucleus during oxidative stress-induced G2 arrest.
  • AMPK inhibition abolished G2 arrest, increased CDK1 activity, and decreased p53/p21 levels.
  • Bypassing G2 arrest led to increased DNA damage, apoptosis, and reduced embryo development.

Conclusions:

  • The G2/M checkpoint and DNA repair are active in mouse zygotes responding to mild oxidative stress.
  • AMPK activation is crucial for regulating oxidative stress-induced G2 arrest by inhibiting CDK1 activity through the p53/p21 pathway.
  • This process facilitates DNA repair, promoting the development and survival of embryos affected by oxidative stress.