Abstract
N6-methyladenosine (m6A) is a well-known post-transcriptional modification that is the most common type of methylation in eukaryotic mRNAs. The regulation of m6A is dynamic and reversible, which is erected by m6A methyltransferases (“writers”) and removed by m6A demethylases (“erasers”). Notably, the effects on targeted mRNAs resulted by m6A predominantly depend on the functions of different m6A-binding proteins (“readers”) including YT521-B homology (YTH) domain family, heterogeneous nuclear ribonucleoproteins (HNRNPs), and insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs). Indeed, m6A readers not only participate in multiple procedures of RNA metabolism, but also are involved in a variety of biological processes. In this review, we summarized the specific functions and underlying mechanisms of m6A-binding proteins in tumorigenesis, hematopoiesis, virus replication, immune response, and adipogenesis.
Highlights
Epigenetic abnormalities, such as DNA methylation, histone modification, genomic imprinting, and chromosome remodeling, mainly affect the characteristics and functions of genes through regulating the transcription or translation processes [1], without altering the DNA sequences
The effects of m6A modification on RNA metabolism predominantly depend on the recognition by different m6A-binding proteins, including but not limited to YT521-B homology (YTH) domain family, heterogeneous nuclear ribonucleoproteins (HNRNPs), and insulin-like growth factor 2 messenger RNAs (mRNAs)-binding proteins (IGF2BPs)
It was noteworthy that the suppression of Human immunodeficiency virus (HIV)-1 reverse transcription and promotion of Gag processing were both triggered by YT521-B homology domain family (YTHDF), which implied the complicated roles of m6A in viral infection [87]
Summary
Epigenetic abnormalities, such as DNA methylation, histone modification, genomic imprinting, and chromosome remodeling, mainly affect the characteristics and functions of genes through regulating the transcription or translation processes [1], without altering the DNA sequences. YTHDF2, the first identified m6A reader, promotes mRNAs degradation and reduces the stability of targeted transcripts through recruiting the CCR4-NOT deadenylase complex [19, 20].
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