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MicroRNA regulation via DNA methylation during the morula to blastocyst transition in mice

Yee-Ming Lee1, Huei-Wen Chen, Pawan Kumar Maurya

  • 1Institute of Pharmacology, College of Medicine, National Yang-Ming University, Taipei, Taiwan.

Molecular Human Reproduction
|November 5, 2011
PubMed

Insights

DNA methylation changes affect microRNA profiles during early mouse embryo development. Inhibiting DNA methylation disrupted embryo development and altered microRNA expression, impacting gene targets crucial for development.

Area of Science:

  • Developmental Biology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic regulation, including DNA methylation, plays a critical role in gene silencing and parental imprinting.
  • MicroRNAs (miRNAs) are key regulators of gene expression, influencing various biological processes.

Purpose of the Study:

  • To investigate the impact of DNA methylation on microRNA expression during the morula-blastocyst transition in mouse embryos.
  • To explore the relationship between epigenetic intervention, microRNA regulation, and fertility.

Main Methods:

  • Mouse embryos were treated with 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhibitor, at varying concentrations.
  • MicroRNA expression changes were quantified using quantitative real-time (Q-PCR)-based megaplex pre-amp microRNA assays.
  • Predicted microRNA targets were identified using bioinformatics tools and confirmed via Q-PCR.

Main Results:

  • 5-aza-dC treatment inhibited mouse embryo development from morula to blastocyst in a dose-dependent manner, with significant arrest at 50 nM.
  • A total of 48 down-regulated and 17 up-regulated microRNAs (≥5-fold change) were identified following 5-aza-dC treatment.
  • Eight key targets, including dnmt3a and jagged 1, were confirmed for the affected microRNAs.

Conclusions:

  • DNA methylation status significantly influences microRNA profiles during the critical morula to blastocyst developmental stage.
  • Altered microRNA expression and identified targets provide insights into the mechanisms linking epigenetic regulation, fertility, and potential interventions.

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