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Local translation under epitranscriptomic control.

José R Sotelo-Silveira1

  • 1Departamento de Genómica, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, 11600, Uruguay; Departamento de Biología Celular y Molecular, Facultad de Ciencias, Universidad de la República, Montevideo, 11400, Uruguay.

Trends in Neurosciences
|October 1, 2025
PubMed
Summary

N6-methyladenosine (m6A) RNA modification regulates local protein translation and axon growth. Specific genetic variants linked to autism and schizophrenia disrupt this process, affecting neurodevelopment.

Keywords:
APCaxonm(6)Aneurodevelopmental disordersproteostasisβ-actin

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Area of Science:

  • Molecular Biology
  • Neuroscience
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) is a prevalent RNA modification influencing gene expression.
  • Local translation of RNA-binding proteins is crucial for cellular processes like axon growth.
  • Disruptions in neurodevelopment are often linked to genetic factors affecting neuronal function.

Purpose of the Study:

  • To investigate the role of m6A RNA modification in controlling local translation of the RNA-binding protein APC.
  • To elucidate the mechanism coupling RNA modification to mRNA translation and axon development.
  • To examine the impact of autism- and schizophrenia-associated METTL14 variants on this pathway.

Main Methods:

  • Utilized techniques to study m6A RNA modification and its effect on protein translation.
  • Investigated the interaction between YTHDF1 and APC.
  • Analyzed the consequences of METTL14 variants on YTHDF1-APC binding and axon length.

Main Results:

  • m6A modification controls local APC translation via YTHDF1.
  • This process links RNA modification to β-actin mRNA translation and axon growth.
  • Autism/schizophrenia-associated METTL14 variants impair YTHDF1-APC binding, reduce APC levels, and shorten axons.

Conclusions:

  • m6A-mediated regulation of APC translation is vital for normal axon development.
  • METTL14 variants associated with neurodevelopmental disorders disrupt this critical pathway.
  • These findings highlight a molecular mechanism underlying autism and schizophrenia.