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The Role of Dynamic m 6 A RNA Methylation in Photobiology
Author(s) -
Robinson Myles,
Shah Palak,
Cui YanHong,
He YuYing
Publication year - 2018
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12930
Subject(s) - biology , demethylase , rna , rna methylation , n6 methyladenosine , rna splicing , microbiology and biotechnology , post transcriptional regulation , methylation , rna binding protein , epigenetics , rna editing , microrna , effector , messenger rna , regulation of gene expression , alternative splicing , methyltransferase , genetics , gene
N 6 ‐methyladenosine (m 6 A) is the most abundant internal RNA modification among numerous post‐transcriptional modifications identified in eukaryotic mRNA . m 6 A modification of RNA is catalyzed by the “writer” m 6 A methyltransferase enzyme complex, consisting of METTL 3, METTL 14, WTAP and KIAA 1429. The m 6 A modification is reversible and can be removed by “eraser” m 6 A demethylase enzymes, namely, FTO and ALKBH 5. The biological function of m 6 A modification on RNA is carried out by RNA ‐binding effector proteins called “readers.” Varied functions of the reader proteins regulate mRNA metabolism by affecting stability, translation, splicing or nuclear export. The epitranscriptomic gene regulation by m 6 A RNA methylation regulates various pathways, which contribute to basic cellular processes essential for cell maintenance, development and cell fate, and affect response to external stimuli and stressors. In this review, we summarize the recent advances in the regulation and function of m 6 A RNA methylation, with a focus on UV ‐induced DNA damage response and the circadian clock machinery. Insights into the mechanisms of m 6 A RNA regulation and post‐transcriptional regulatory function in these biological processes may facilitate the development of new preventive and therapeutic strategies for various diseases related to dysregulation of UV damage response and circadian rhythm.

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