Special Issue "R-loop Biology in Eukaryotes"

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics".

Deadline for manuscript submissions: closed (31 March 2017)

Special Issue Editor

Guest Editor
Prof. Dr. Frédéric Chédin

Department of Molecular and Cellular Biology, University of California Davis, Davis, CA 95616, USA
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Special Issue Information

Dear Colleagues,

Over the past decade, our understanding of the biology of R-loop structures in Eukaryotes has made tremendous progress. We now know that R-loop formation is a prevalent and dynamic component of the eukaryotic chromatin that is subject to careful regulation in time and space. Accumulating evidence has convincingly linked R-loop structures to numerous nuclear processes including transcription, DNA replication, DNA repair, DNA recombination, and chromatin patterning. Not surprisingly, perturbations in R-loop metabolism cause various forms of nuclear stress and have been linked to multiple human diseases. In recognition of this progress, we would like to commission what is likely to be the first book focused on this topic. The goal of this special issue of Genes is to provide both newcomers and experts a comprehensive and up to date overview of the field, its progress, its challenges, and its future. Proposed topics for the series will cover both model organisms and mammalian systems including humans. A non-exhaustive list of topics to be covered will include global R-loop mapping, analysis of R-loop formation and resolution pathways, links between perturbations in R-loop homeostasis and genomic instabilility, possible physiological roles of R-loop structures in chromatin patterning, transcriptional control, and recombination initiation as well as roles for R-loop dysfunction in human diseases.

We welcome your participation in this exciting endeavor and hope you will contribute your expertise in the form of a review or original article.

Prof. Dr. Frédéric Chédin
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 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.

Keywords

  • R-loop
  • transcription
  • chromatin
  • genomic instability
  • DNA breaks
  • disease

Published Papers (4 papers)

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Review

Open AccessReview The Role of Replication-Associated Repair Factors on R-Loops
Genes 2017, 8(7), 171; doi:10.3390/genes8070171
Received: 4 May 2017 / Revised: 19 June 2017 / Accepted: 20 June 2017 / Published: 27 June 2017
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Abstract
The nascent RNA can reinvade the DNA double helix to form a structure termed the R-loop, where a single-stranded DNA (ssDNA) is accompanied by a DNA-RNA hybrid. Unresolved R-loops can impede transcription and replication processes and lead to genomic instability by a mechanism
[...] Read more.
The nascent RNA can reinvade the DNA double helix to form a structure termed the R-loop, where a single-stranded DNA (ssDNA) is accompanied by a DNA-RNA hybrid. Unresolved R-loops can impede transcription and replication processes and lead to genomic instability by a mechanism still not fully understood. In this sense, a connection between R-loops and certain chromatin markers has been reported that might play a key role in R-loop homeostasis and genome instability. To counteract the potential harmful effect of R-loops, different conserved messenger ribonucleoprotein (mRNP) biogenesis and nuclear export factors prevent R-loop formation, while ubiquitously-expressed specific ribonucleases and DNA-RNA helicases resolve DNA-RNA hybrids. However, the molecular events associated with R-loop sensing and processing are not yet known. Given that R-loops hinder replication progression, it is plausible that some DNA replication-associated factors contribute to dissolve R-loops or prevent R-loop mediated genome instability. In support of this, R-loops accumulate in cells depleted of the BRCA1, BRCA2 or the Fanconi anemia (FA) DNA repair factors, indicating that they play an active role in R-loop dissolution. In light of these results, we review our current view of the role of replication-associated DNA repair pathways in preventing the harmful consequences of R-loops. Full article
(This article belongs to the Special Issue R-loop Biology in Eukaryotes)
Figures

Figure 1

Open AccessReview Ataxin-2: From RNA Control to Human Health and Disease
Genes 2017, 8(6), 157; doi:10.3390/genes8060157
Received: 1 March 2017 / Revised: 23 May 2017 / Accepted: 31 May 2017 / Published: 5 June 2017
Cited by 1 | PDF Full-text (1244 KB) | HTML Full-text | XML Full-text
Abstract
RNA-binding proteins play fundamental roles in the regulation of molecular processes critical to cellular and organismal homeostasis. Recent studies have identified the RNA-binding protein Ataxin-2 as a genetic determinant or risk factor for various diseases including spinocerebellar ataxia type II (SCA2) and amyotrophic
[...] Read more.
RNA-binding proteins play fundamental roles in the regulation of molecular processes critical to cellular and organismal homeostasis. Recent studies have identified the RNA-binding protein Ataxin-2 as a genetic determinant or risk factor for various diseases including spinocerebellar ataxia type II (SCA2) and amyotrophic lateral sclerosis (ALS), amongst others. Here, we first discuss the increasingly wide-ranging molecular functions of Ataxin-2, from the regulation of RNA stability and translation to the repression of deleterious accumulation of the RNA-DNA hybrid-harbouring R-loop structures. We also highlight the broader physiological roles of Ataxin-2 such as in the regulation of cellular metabolism and circadian rhythms. Finally, we discuss insight from clinically focused studies to shed light on the impact of molecular and physiological roles of Ataxin-2 in various human diseases. We anticipate that deciphering the fundamental functions of Ataxin-2 will uncover unique approaches to help cure or control debilitating and lethal human diseases. Full article
(This article belongs to the Special Issue R-loop Biology in Eukaryotes)
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Figure 1

Open AccessReview R Loops in the Regulation of Antibody Gene Diversification
Genes 2017, 8(6), 154; doi:10.3390/genes8060154
Received: 28 March 2017 / Revised: 24 May 2017 / Accepted: 31 May 2017 / Published: 2 June 2017
PDF Full-text (561 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
For nearly three decades, R loops have been closely linked with class switch recombination (CSR), the process that generates antibody isotypes and that occurs via a complex cascade initiated by transcription-coupled mutagenesis in switch recombination sequences. R loops form during transcription of switch
[...] Read more.
For nearly three decades, R loops have been closely linked with class switch recombination (CSR), the process that generates antibody isotypes and that occurs via a complex cascade initiated by transcription-coupled mutagenesis in switch recombination sequences. R loops form during transcription of switch recombination sequences in vitro and in vivo, and there is solid evidence that R loops are required for efficient class switching. The classical model of R loops posits that they boost mutation rates by generating stable and long tracts of single-stranded DNA that serve as the substrate for activation induced deaminase (AID), the enzyme that initiates the CSR reaction cascade by co-transcriptionally mutating ssDNA in switch recombination sequences. Though logical and compelling, this model has not been supported by in vivo evidence. Indeed, several reports suggest that R loops may not be involved in recruiting AID activity to switch regions, meaning that R loops probably serve other unanticipated roles in CSR. Here, I review the key findings in this field to date and propose hypotheses that could help towards elucidating the precise function of R loops in CSR. Full article
(This article belongs to the Special Issue R-loop Biology in Eukaryotes)
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Figure 1

Open AccessReview Replication Fork Protection Factors Controlling R-Loop Bypass and Suppression
Genes 2017, 8(1), 33; doi:10.3390/genes8010033
Received: 28 October 2016 / Revised: 2 January 2017 / Accepted: 9 January 2017 / Published: 14 January 2017
Cited by 5 | PDF Full-text (557 KB) | HTML Full-text | XML Full-text
Abstract
Replication–transcription conflicts have been a well-studied source of genome instability for many years and have frequently been linked to defects in RNA processing. However, recent characterization of replication fork-associated proteins has revealed that defects in fork protection can directly or indirectly stabilize R-loop
[...] Read more.
Replication–transcription conflicts have been a well-studied source of genome instability for many years and have frequently been linked to defects in RNA processing. However, recent characterization of replication fork-associated proteins has revealed that defects in fork protection can directly or indirectly stabilize R-loop structures in the genome and promote transcription–replication conflicts that lead to genome instability. Defects in essential DNA replication-associated activities like topoisomerase, or the minichromosome maintenance (MCM) helicase complex, as well as fork-associated protection factors like the Fanconi anemia pathway, both appear to mitigate transcription–replication conflicts. Here, we will highlight recent advances that support the concept that normal and robust replisome function itself is a key component of mitigating R-loop coupled genome instability. Full article
(This article belongs to the Special Issue R-loop Biology in Eukaryotes)
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