mRNA mA methylation downregulates adipogenesis in porcine adipocytes

Xinxia Wang1, Linna Zhu1, Jingqing Chen1

  • 1College of Animal Sciences, Zhejiang University, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China; Key Laboratory of Animal Nutrition & Feed Sciences, Ministry of Agriculture, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China; Zhejiang Provincial Laboratory of Feed and Animal Nutrition, No. 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.

Insights

The study reveals that N6-methyladenosine (m(6)A) plays a crucial role in fat cell development (adipogenesis). Modulating m(6)A levels impacts fat accumulation, offering insights into obesity regulation.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cell Biology

Background:

  • The Fat Mass and Obesity-associated protein (FTO) is linked to obesity and demethylates N6-methyladenosine (m(6)A).
  • The precise role of m(6)A in adipogenesis remains unclear, prompting further investigation.

Purpose of the Study:

  • To elucidate the role of m(6)A in regulating adipogenesis.
  • To investigate the opposing effects of FTO and METTL3 on m(6)A levels and adipogenesis.

Main Methods:

  • Overexpression and knockdown of FTO and METTL3 in porcine adipocytes.
  • Chemical treatment using methylation inhibitor cycloleucine and methyl donor betaine.
  • Assessment of m(6)A levels and lipid accumulation.

Main Results:

  • FTO negatively regulated m(6)A levels and promoted adipogenesis.
  • METTL3 positively correlated with m(6)A levels and inhibited adipogenesis.
  • m(6)A demonstrated an inverse effect on lipid accumulation in porcine adipocytes.

Conclusions:

  • m(6)A is a critical regulator of adipogenesis.
  • FTO and METTL3 have opposing roles in m(6)A-mediated adipogenesis.
  • Findings provide a basis for understanding obesity through epigenetic mechanisms.