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DMSO impairs the transcriptional program for maternal-to-embryonic transition by altering histone acetylation

Min-Hee Kang1, Seong-Yeob You1, Kwonho Hong1

  • 1Department of Stem Cell and Regenerative Biotechnology, Humanized Pig Research Center (SRC), Konkuk University, Seoul, South Korea.

Biomaterials
|November 26, 2019
PubMed

Insights

Dimethyl sulfoxide (DMSO) causes mouse embryo developmental arrest by disrupting the maternal-to-embryonic transition. This solvent affects gene expression and epigenetic modifications, highlighting toxicity concerns in research.

Area of Science:

  • Developmental Biology
  • Epigenetics
  • Toxicology

Background:

  • Dimethyl sulfoxide (DMSO) is a common solvent in research.
  • Its effects on early embryonic development and epigenetics are not fully understood.

Purpose of the Study:

  • To investigate the impact of DMSO on mouse zygote development and transcriptional programs.
  • To elucidate the epigenetic mechanisms underlying DMSO-induced developmental toxicity.

Main Methods:

  • Exposure of mouse zygotes to 2% DMSO.
  • Analysis of transcriptional changes and epigenetic modifications (protein acetylation, histone acetylation).
  • Assessment of embryonic development up to the 4-cell stage.

Main Results:

  • 2% DMSO exposure caused developmental arrest at the 2- or 4-cell stage in mouse embryos.
  • DMSO altered global protein acetylation and specific histone modifications (H3, H4, H3K9, H3K27).
  • Significant changes in gene expression were observed, affecting maternal, zygotic gene activation (ZGA), cell cycle, and ribosomal biogenesis genes.

Conclusions:

  • DMSO disrupts the maternal-to-embryonic transition, leading to developmental arrest.
  • Epigenetic alterations are a key mechanism of DMSO toxicity in early embryogenesis.
  • Caution is advised when using DMSO as a solvent in research involving embryos.
Keywords:
2-cell blockAcetylationDMSOEpigeneticsMouse preimplantation embryoRNA-Seq

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