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Mettl14 Deficiency Promotes Fam32a Expression via m6A Modifications to Facilitate the Hepatocyte G1/S Transition

Chengyu Li1, Wenhan Zhou1, Dayu Wang2

  • 1College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.

Journal of Cellular Physiology
|October 16, 2025
PubMed

Insights

Mettl14 deficiency stabilizes Fam32a mRNA via m6A modifications, increasing Fam32a protein and accelerating hepatocyte cell cycle G1/S transition by altering Cdkn1a splicing.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Hepatology

Background:

  • Mettl14 is vital for the m6A methyltransferase complex, impacting mRNA stability and splicing.
  • Reduced Mettl14 expression links to hepatocellular carcinoma and liver regeneration.
  • Mechanisms of Mettl14 in hepatocyte cell cycle regulation are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms of Mettl14 in regulating hepatocyte cell cycle progression.
  • To investigate the role of m6A modifications in Mettl14-mediated cell cycle control.

Main Methods:

  • RNA-sequencing (RNA-Seq) and m6A immunoprecipitation sequencing (MeRIP-Seq) were performed in liver-specific Mettl14 knockout mice.
  • Analysis focused on mRNA stability, protein levels, and alternative splicing events.

Main Results:

  • Mettl14 deficiency led to stabilization of Fam32a mRNA through m6A modifications, increasing Fam32a protein levels.
  • Elevated Fam32a expression was found to accelerate the G1/S transition in hepatocytes.
  • This acceleration was linked to modulated Cdkn1a splicing, specifically downregulating its variant 2.

Conclusions:

  • A novel m6A-dependent pathway regulating hepatocyte cell cycle progression was uncovered.
  • Fam32a plays a previously unrecognized role in promoting the G1/S transition.
  • Mettl14's function in liver cell cycle control is mediated, in part, by Fam32a and Cdkn1a splicing.
Keywords:
Cdkn1aFam32aG1/S transitionRNA splicingm6A

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