Advances in Profiling and Deciphering the Functional Role of RNA Modifications

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 4878

Special Issue Editors


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Guest Editor
Center for Genomic Science, Istituto Italiano di Tecnologia, 16163 Genova, Italy
Interests: gene expression; genomics; bioinformatics and computational biology; gene regulation; bioinformatics; epigenetics; transcriptomics; computational biology; transcription; NGS data analysis; DNA methylation; RNA methylation; epitranscriptome; RNA metabolism; gene expression and chromatin biology; chromatin; methylation; epigenomics

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Guest Editor
Core Research Laboratory - Istituto Toscano TumoriAzienda Ospedaliero, Universitaria Careggiviale G. Pieraccini 6, Firenze, Italy
Interests: DNA and RNA editing

Special Issue Information

Dear Colleagues,

In parallel to the surge of studies in the field of epigenetics, dozens of epitranscriptional RNA modifications were identified in the last decades. Research in the epitranscriptome field has benefited from the recent development of methods to better quantify these marks and profile them at the genome level. Yet, despite a number of studies have confirmed the prominent role of some of these marks in shaping the fate of marked RNAs, we are only at the beginning of deciphering the effects of these modifications. Multiple effectors were identified that contribute to installing, removing, and reading these marks. However, the detailed activity of individual effectors and their joint contribution to the establishment of specific epitranscriptional patterns are yet to be deciphered. As the field progresses, novel methods are awaited for the specific, quantitative, and high-resolution profiling of these marks. Eventually, these maps will start revealing the functional role of individual modifications in physiological and disease conditions and whether the ensemble of modifications decorating various transcript types defines a new epitranscriptional code.

In this Special Issue, we will consider outstanding reviews, research, or method manuscripts on the following topics:

  • Experimental methods to profile RNA modifications
  • Computational methods for the analysis of epitranscriptional data
  • Insights on the functional role of epitranscriptional marks and their effectors
  • Prevalence and functional role of epitranscriptional marks in diseases
  • The crosstalk between epitranscriptional marks
  • The crosstalk between the epitranscriptome and the epigenome

Dr. Mattia Pelizzola
Dr. Silvo Conticello
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Epigenomes is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (1 paper)

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Research

12 pages, 1673 KiB  
Article
Implication of m6A mRNA Methylation in Susceptibility to Inflammatory Bowel Disease
by Maialen Sebastian-delaCruz, Ane Olazagoitia-Garmendia, Itziar Gonzalez-Moro, Izortze Santin, Koldo Garcia-Etxebarria and Ainara Castellanos-Rubio
Epigenomes 2020, 4(3), 16; https://0-doi-org.brum.beds.ac.uk/10.3390/epigenomes4030016 - 03 Aug 2020
Cited by 19 | Viewed by 4167
Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract that develops due to the interaction between genetic and environmental factors. More than 160 loci have been associated with IBD, but the functional implication of many of the associated genes [...] Read more.
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract that develops due to the interaction between genetic and environmental factors. More than 160 loci have been associated with IBD, but the functional implication of many of the associated genes remains unclear. N6-Methyladenosine (m6A) is the most abundant internal modification in mRNA. m6A methylation regulates many aspects of mRNA metabolism, playing important roles in the development of several pathologies. Interestingly, SNPs located near or within m6A motifs have been proposed as possible contributors to disease pathogenesis. We hypothesized that certain IBD-associated SNPs could regulate the function of genes involved in IBD development via m6A-dependent mechanisms. We used online available GWAS, m6A and transcriptome data to find differentially expressed genes that harbored m6A-SNPs associated with IBD. Our analysis resulted in five candidate genes corresponding to two of the major IBD subtypes: UBE2L3 and SLC22A4 for Crohn’s Disease and TCF19, C6orf47 and SNAPC4 for Ulcerative Colitis. Further analysis using in silico predictions and co-expression analyses in combination with in vitro functional studies showed that our candidate genes seem to be regulated by m6A-dependent mechanisms. These findings provide the first indication of the implication of RNA methylation events in IBD pathogenesis. Full article
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