METTL1 Promotes let-7 MicroRNA Processing via m7G Methylation.
7-methylguanosine
G-quadruplexes
METTL1
RNA methylation
SAM-dependent methyltransferase
cell migration
high-throughput sequencing
let-7
miRNA biogenesis
microRNA
Journal
Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571
Informations de publication
Date de publication:
20 06 2019
20 06 2019
Historique:
received:
18
04
2018
revised:
06
03
2019
accepted:
27
03
2019
pubmed:
30
4
2019
medline:
14
1
2020
entrez:
30
4
2019
Statut:
ppublish
Résumé
7-methylguanosine (m7G) is present at mRNA caps and at defined internal positions within tRNAs and rRNAs. However, its detection within low-abundance mRNAs and microRNAs (miRNAs) has been hampered by a lack of sensitive detection strategies. Here, we adapt a chemical reactivity assay to detect internal m7G in miRNAs. Using this technique (Borohydride Reduction sequencing [BoRed-seq]) alongside RNA immunoprecipitation, we identify m7G within a subset of miRNAs that inhibit cell migration. We show that the METTL1 methyltransferase mediates m7G methylation within miRNAs and that this enzyme regulates cell migration via its catalytic activity. Using refined mass spectrometry methods, we map m7G to a single guanosine within the let-7e-5p miRNA. We show that METTL1-mediated methylation augments let-7 miRNA processing by disrupting an inhibitory secondary structure within the primary miRNA transcript (pri-miRNA). These results identify METTL1-dependent N7-methylation of guanosine as a new RNA modification pathway that regulates miRNA structure, biogenesis, and cell migration.
Identifiants
pubmed: 31031083
pii: S1097-2765(19)30269-2
doi: 10.1016/j.molcel.2019.03.040
pmc: PMC6591002
pii:
doi:
Substances chimiques
MicroRNAs
0
mirnlet7 microRNA, human
0
Guanosine
12133JR80S
7-methylguanosine
2140-77-4
METTL1 protein, human
EC 2.1.1.-
Methyltransferases
EC 2.1.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1278-1290.e9Subventions
Organisme : Cancer Research UK
Pays : United Kingdom
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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