RNA m6A methylation across the transcriptome.

Mol Cell

Ludwig Institute for Cancer Research, University of Oxford, Roosevelt Dr, Headington, Oxford OX3 7DQ, UK. Electronic address:

Published: February 2023

AI Article Synopsis

  • N6-methyl adenosine (m6A) is a prevalent chemical modification found on both coding and non-coding RNAs in mammalian cells, linked to specific evolutionary enzymes.
  • Recent research highlights m6A's significant role in regulating gene expression and chromatin states within the nucleus.
  • Further studies are essential to explore how m6A impacts various biological processes and its implications for health and disease.

Article Abstract

Since the early days of foundational studies of nucleic acids, many chemical moieties have been discovered to decorate RNA and DNA in diverse organisms. In mammalian cells, one of these chemical modifications, N6-methyl adenosine (m6A), is unique in a way that it is highly abundant not only on RNA polymerase II (RNAPII) transcribed, protein-coding transcripts but also on non-coding RNAs, such as ribosomal RNAs and snRNAs, mediated by distinct, evolutionarily conserved enzymes. Here, we review RNA m6A modification in the light of the recent appreciation of nuclear roles for m6A in regulating chromatin states and gene expression, as well as the recent discoveries of the evolutionarily conserved methyltransferases, which catalyze methylation of adenosine on diverse sets of RNAs. Considering that the substrates of these enzymes are involved in many important biological processes, this modification warrants further research to understand the molecular mechanisms and functions of m6A in health and disease.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.molcel.2023.01.006DOI Listing

Publication Analysis

Top Keywords

rna m6a
8
evolutionarily conserved
8
rna
4
m6a methylation
4
methylation transcriptome
4
transcriptome early
4
early days
4
days foundational
4
foundational studies
4
studies nucleic
4

Similar Publications

Reduced trophoblast migration and invasion contribute to unexplained recurrent spontaneous abortion (URSA). Aquaporin 3 (AQP3) plays a crucial role in facilitating trophoblast migration and invasion during early pregnancy through fetal-maternal crosstalk. This study aimed to comprehensively investigate the mechanism involving AQP3 and its modulatory effects on human extravillous trophoblast (HTR-8/SVneo cells) migration and invasion.

View Article and Find Full Text PDF

Background: Post-menopausal women experience more severe muscular fatty infiltration, though the mechanisms remain unclear. The decline in estrogen levels is considered as a critical physiological alteration during post-menopause. Fibro/adipogenic progenitors (FAPs) are identified as major contributors to muscular fatty infiltration.

View Article and Find Full Text PDF

Esketamine, a newly developed antidepressant, is the subject of this research which seeks to explore its impact on depressive symptoms in neuropathic pain mice and the potential molecular mechanisms involved. Through transcriptome sequencing and bioinformatics analysis combined with in vivo studies, it was identified that esketamine markedly boosts the levels of the m6A methyltransferase METTL3 and the AMPA receptor GluA1 subunit. Esketamine activates METTL3, allowing it to bind with GluA1 mRNA, promoting m6A modification, thereby enhancing GluA1 expression at synapses.

View Article and Find Full Text PDF

Introduction: Spinal cord injury (SCI) is a severe central nervous system disorder with limited treatment options. While autophagy plays a protective role in neural repair, its regulatory mechanisms in SCI remain unclear. Actin-like protein 6A (Actl6a) influences cell fate and neural development, yet its specific role in SCI repair is not well understood.

View Article and Find Full Text PDF

m6A modified ATG9A is required in regulating autophagy to promote HSCs activation and liver fibrosis.

Cell Signal

January 2025

Department of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China. Electronic address:

Hepatic stellate cells (HSCs) are the central link of the occurrence and development of hepatic fibrosis, and autophagy promotes HSCs activation. N6-methyladenosine (m6A) RNA modification can also control autophagy by targeting selected autophagy-associated genes. but up to now, little research has been done on the m6A modification autophagy-related genes (ATGs) in hepatic fibrosis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!