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MeCP2 Governs maternal hyperandrogenism-induced cortical defects and behavioral alterations via noncanonical

Yu-Meng Wang1,2, Yanyan Jia3, Yu Wu4

  • 1Department of Cardiology, Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. yumeng1229@126.com.

Nature Communications
|May 13, 2026
PubMed

Insights

Elevated prenatal androgens disrupt male brain development via a novel pathway involving MeCP2 and MEF2C. Blocking androgen receptors (AR) or key genes reversed these neurodevelopmental and behavioral changes.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Endocrinology

Background:

  • Prenatal androgen exposure is linked to neurodevelopmental conditions.
  • Mechanisms underlying this association are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which elevated prenatal androgens affect cortical development and behavior.
  • To investigate the role of androgen receptors (AR) and MeCP2 in mediating these effects.

Main Methods:

  • Aromatase inhibition in mice to model elevated prenatal androgens.
  • Analysis of cortical development and behavior in male offspring.
  • Gene knockdown experiments (Mecp2, Mef2c) and AR blockade.
  • Investigation of MeCP2 duplication models.

Main Results:

  • Elevated prenatal androgens disrupt cortical development and behavior in male mice.
  • Androgen receptor (AR) activation upregulates MEF2C via interaction with MeCP2, bypassing canonical androgen response elements.
  • Knocking down Mecp2 or Mef2c, or blocking AR, reversed the androgen-induced effects.
  • Mecp2 duplication alone caused similar neurogenesis and behavioral changes, reversible by AR blockade.

Conclusions:

  • A non-canonical, MeCP2-mediated pathway links prenatal androgens to male-biased neurodevelopmental conditions.
  • This pathway involves AR-MeCP2 interaction to upregulate MEF2C, impacting neurogenesis and behavior.
  • Targeting AR may offer therapeutic strategies for androgen-associated neurodevelopmental disorders.

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