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Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration

N6-methyladenosine (m(6)A), the most abundant modification in messenger RNAs (mRNAs), is deposited by methyltransferases (“writers”) Mettl3 and Mettl14 and erased by demethylases (“erasers”) Fto and Alkbh5. m(6)A can be recognized by m(6)A-binding proteins (“readers”), such as Yth domain family prot...

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Autores principales: Shu, Liqi, Huang, Xiaoli, Cheng, Xuejun, Li, Xuekun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8534826/
https://www.ncbi.nlm.nih.gov/pubmed/34685675
http://dx.doi.org/10.3390/cells10102694
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author Shu, Liqi
Huang, Xiaoli
Cheng, Xuejun
Li, Xuekun
author_facet Shu, Liqi
Huang, Xiaoli
Cheng, Xuejun
Li, Xuekun
author_sort Shu, Liqi
collection PubMed
description N6-methyladenosine (m(6)A), the most abundant modification in messenger RNAs (mRNAs), is deposited by methyltransferases (“writers”) Mettl3 and Mettl14 and erased by demethylases (“erasers”) Fto and Alkbh5. m(6)A can be recognized by m(6)A-binding proteins (“readers”), such as Yth domain family proteins (Ythdfs) and Yth domain-containing protein 1 (Ythdc1). Previous studies have indicated that m(6)A plays an essential function in various fundamental biological processes, including neurogenesis and neuronal development. Dysregulated m(6)A modification contributes to neurological disorders, including neurodegenerative diseases. In this review, we summarize the current knowledge about the roles of m(6)A machinery, including writers, erasers, and readers, in regulating gene expression and the function of m(6)A in neurodevelopment and neurodegeneration. We also discuss the perspectives for studying m(6)A methylation.
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spelling pubmed-85348262021-10-23 Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration Shu, Liqi Huang, Xiaoli Cheng, Xuejun Li, Xuekun Cells Review N6-methyladenosine (m(6)A), the most abundant modification in messenger RNAs (mRNAs), is deposited by methyltransferases (“writers”) Mettl3 and Mettl14 and erased by demethylases (“erasers”) Fto and Alkbh5. m(6)A can be recognized by m(6)A-binding proteins (“readers”), such as Yth domain family proteins (Ythdfs) and Yth domain-containing protein 1 (Ythdc1). Previous studies have indicated that m(6)A plays an essential function in various fundamental biological processes, including neurogenesis and neuronal development. Dysregulated m(6)A modification contributes to neurological disorders, including neurodegenerative diseases. In this review, we summarize the current knowledge about the roles of m(6)A machinery, including writers, erasers, and readers, in regulating gene expression and the function of m(6)A in neurodevelopment and neurodegeneration. We also discuss the perspectives for studying m(6)A methylation. MDPI 2021-10-09 /pmc/articles/PMC8534826/ /pubmed/34685675 http://dx.doi.org/10.3390/cells10102694 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Shu, Liqi
Huang, Xiaoli
Cheng, Xuejun
Li, Xuekun
Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
title Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
title_full Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
title_fullStr Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
title_full_unstemmed Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
title_short Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
title_sort emerging roles of n6-methyladenosine modification in neurodevelopment and neurodegeneration
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8534826/
https://www.ncbi.nlm.nih.gov/pubmed/34685675
http://dx.doi.org/10.3390/cells10102694
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