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m6A in the Signal Transduction Network

  • Jang, Ki-Hong (Department of Microbiology and Molecular Genetics, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine) ;
  • Heras, Chloe R. (Department of Microbiology and Molecular Genetics, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine) ;
  • Lee, Gina (Department of Microbiology and Molecular Genetics, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine)
  • Received : 2022.02.02
  • Accepted : 2022.03.23
  • Published : 2022.07.31

Abstract

In response to environmental changes, signaling pathways rewire gene expression programs through transcription factors. Epigenetic modification of the transcribed RNA can be another layer of gene expression regulation. N6-adenosine methylation (m6A) is one of the most common modifications on mRNA. It is a reversible chemical mark catalyzed by the enzymes that deposit and remove methyl groups. m6A recruits effector proteins that determine the fate of mRNAs through changes in splicing, cellular localization, stability, and translation efficiency. Emerging evidence shows that key signal transduction pathways including TGFβ (transforming growth factor-β), ERK (extracellular signal-regulated kinase), and mTORC1 (mechanistic target of rapamycin complex 1) regulate downstream gene expression through m6A processing. Conversely, m6A can modulate the activity of signal transduction networks via m6A modification of signaling pathway genes or by acting as a ligand for receptors. In this review, we discuss the current understanding of the crosstalk between m6A and signaling pathways and its implication for biological systems.

Keywords

Acknowledgement

We thank members of the Lee laboratory for helpful discussions, especially Laurence Seabrook, Yujin Chun, and Sunhee Jung, for their feedback on the manuscript. We apologize to authors whose work was not cited due to space limitations. This work was supported by the Department of Defense grant TS200022.

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