Abstract
N6-methyladenosine (m6A) is a widespread posttranscriptional RNA modification that occurs in tRNA, rRNA, snRNA, viral RNAs, and more recently is shown to occur in mRNA in a dynamic, reversible manner. At the epicenter of RNA epigenetics, m6A influences essentially all stages of RNA metabolism. As a result, m6A modulates cell differentiation and pluripotency, cell cycle and tumorigenesis, and several types of stress responses, etc. A recent report by Shi and colleagues uncovers a novel pathway in which m6A RNA, its associated enzymes, and DNA polymerase κ constitute an early-response system that confers cellular resistance to ultraviolet irradiation, separate from the canonical nucleotide excision repair (NER) pathway that normally repairs UV-induced DNA damage.
Highlights
Among the trio of linear heteropolymers that enable organic life as we know it, RNAs are recognized as the most versatile and self-sufficient
In order to serve its primary directive in the faithful preservation and propagation of genetic information to subsequent generations, DNA assumes a protective, inert duplex structure where sequence information is carefully concealed in is hydrophobic, stacked central axes
(BER), nucleotide excision repair (NER; Fig. 1), mismatch repair, etc. that act on single-strand damages, as well as non-homologous end joining (NHEJ), microhomologymediated end joining (MMEJ), and homologous recombination (HR), which repair double-strand breaks (DSBs) [1]
Summary
Among the trio of linear heteropolymers that enable organic life as we know it, RNAs are recognized as the most versatile and self-sufficient. The deposition of m6A modification can lead to immediate remodeling of RNA secondary and tertiary structures, as m 6A weakens duplex formation and stabilizes stacking within single-stranded regions.
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