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HDAC6 inhibition induces the failure of mouse early embryonic development

Hui Wang1, Li Ling1, Limei Ai2

  • 1Department of Histology and Embryology, Nanjing Medical University, Nanjing, China.

Journal of Cellular Physiology
|October 30, 2018
PubMed

Insights

Histone deacetylase 6 (HDAC6) inhibition impairs mouse early embryo development by causing chromosomal errors, DNA damage, and apoptosis. This highlights HDAC6

Area of Science:

  • Developmental Biology
  • Epigenetics
  • Cell Biology

Background:

  • Histone deacetylases (HDACs) regulate diverse biological processes.
  • The specific role of HDAC6 in early embryonic development is largely unknown.
  • Understanding HDAC6 function is crucial for reproductive biology and developmental toxicology.

Purpose of the Study:

  • To investigate the function of HDAC6 in mouse early embryonic development.
  • To determine the effects of HDAC6 inhibition on blastocyst formation and embryo quality.

Main Methods:

  • Treatment of mouse embryos with Tubastatin A (TubA), a selective HDAC6 inhibitor.
  • Assessment of blastocyst formation rates.
  • Confocal microscopy for chromosomal analysis.
  • Measurement of reactive oxygen species (ROS) production.
  • Immunofluorescence staining for phosphorylated γH2AX.
  • Apoptosis assays in blastocysts.

Main Results:

  • HDAC6 inhibition significantly reduced blastocyst formation.
  • TubA treatment led to increased chromosomal congression failure and DNA damage (indicated by γH2AX accumulation).
  • HDAC6 inhibition caused overproduction of ROS and increased blastocyst apoptosis.

Conclusions:

  • HDAC6 plays a critical role in maintaining chromatin structure and mitochondrial function during early mouse embryogenesis.
  • HDAC6 is essential for proper chromosome segregation and preventing DNA damage.
  • HDAC6 activity is vital for the developmental potential of early mouse embryos.
Keywords:
apoptosisembryoepigenetichistone deacetylases (HDAC)oxidative stress

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