A Commemorative Issue in Honor of Professor Denise P. Barlow: Genomic Imprinting, Epigenetics and Transcriptional Control

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

Deadline for manuscript submissions: closed (30 November 2018) | Viewed by 11069

Special Issue Editors


E-Mail
Guest Editor
Institute of Science and Technology Austria, Am Campus 1, 3400 Klosterneuburg, Austria
Interests: RNA; genetics; epigenetics; transcription; DNA methylation; genomic imprinting; RNA-Seq; lncRNAs; single-cell; cortex development

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Medical University of Vienna, Vienna, Austria
Interests: embryology; developmental biology; genetics; epigenetics; endometriosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The open access journal Epigenomes is now accepting submissions for this Special Issue on genomic imprinting, epigenetics and transcriptional control, which is a commemorative issue in honor of Professor Dr. Denise P. Barlow. This Special Issue is Guest Edited by Dr. Florian M. Pauler from the Institute of Science and Technology Austria, Austria, and Dr. Quanah J. Hudson, a freelance writer based in Austria.

Denise Barlow was known to many as “a pioneer of genomic imprinting” (Wutz A, EMBO Reports, 2017) and therefore, appropriately, this Special Issue focuses on this epigenetic mechanism, which restricts the expression of a small set of genes to one of the two parental alleles in diploid cells. Her vision was to use genomic imprinting as an “epigenetic discovery model” (Barlow DP, Annu Rev Genet 2011) and following this approach she made major contributions to understanding many aspects of epigenetic transcriptional control. Therefore, we believe it is in her scientific spirit to widen the scope of this issue to “all the weird and wonderful things that can't be explained by genetics.” (Barlow D, RNA Biology Feb, 2015). Denise Barlow loved all aspects of rigorously conducted science, including “negative results” that resolve important questions in a field. Therefore, we encourage submission of review, research and/or methods manuscripts on the following topics:

  • genomic imprinting;
  • long non-coding RNA;
  • epigenetics;
  • transcriptional control
  • histone modifications
  • RNA biology
  • allelic expression

Dr. Florian M. Pauler
Dr. Quanah J. Hudson
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.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 1722 KiB  
Article
An Orphan CpG Island Drives Expression of a let-7 miRNA Precursor with an Important Role in Mouse Development
by Martha V. Koerner, Kashyap Chhatbar, Shaun Webb, Justyna Cholewa-Waclaw, Jim Selfridge, Dina De Sousa, Bill Skarnes, Barry Rosen, Mark Thomas, Joanna Bottomley, Ramiro Ramirez-Solis, Christopher Lelliott, David J. Adams and Adrian Bird
Epigenomes 2019, 3(1), 7; https://doi.org/10.3390/epigenomes3010007 - 13 Mar 2019
Cited by 3 | Viewed by 4610
Abstract
Most human genes are associated with promoters embedded in non-methylated, G + C-rich CpG islands (CGIs). Not all CGIs are found at annotated promoters, however, raising the possibility that many serve as promoters for transcripts that do not code for proteins. To test [...] Read more.
Most human genes are associated with promoters embedded in non-methylated, G + C-rich CpG islands (CGIs). Not all CGIs are found at annotated promoters, however, raising the possibility that many serve as promoters for transcripts that do not code for proteins. To test this hypothesis, we searched for novel transcripts in embryonic stem cells (ESCs) that originate within orphan CGIs. Among several candidates, we detected a transcript that included three members of the let-7 micro-RNA family: Let-7a-1, let-7f-1, and let-7d. Deletion of the CGI prevented expression of the precursor RNA and depleted the included miRNAs. Mice homozygous for this mutation were sub-viable and showed growth and other defects. The results suggest that despite the identity of their seed sequences, members of the let-7 miRNA family exert distinct functions that cannot be complemented by other members. Full article
Show Figures

Figure 1

Review

Jump to: Research

8 pages, 1064 KiB  
Review
The Role of the Prader-Willi Syndrome Critical Interval for Epigenetic Regulation, Transcription and Phenotype
by Simona Zahova and Anthony R. Isles
Epigenomes 2018, 2(4), 18; https://doi.org/10.3390/epigenomes2040018 - 18 Oct 2018
Cited by 3 | Viewed by 5909
Abstract
Prader-Willi Syndrome (PWS) is a neurodevelopmental disorder caused by loss of expression of the paternally inherited genes on chromosome 15q11.2-q13. However, the core features of PWS have been attributed to a critical interval (PWS-cr) within the 15q11.2-q13 imprinted gene cluster, containing the small [...] Read more.
Prader-Willi Syndrome (PWS) is a neurodevelopmental disorder caused by loss of expression of the paternally inherited genes on chromosome 15q11.2-q13. However, the core features of PWS have been attributed to a critical interval (PWS-cr) within the 15q11.2-q13 imprinted gene cluster, containing the small nucleolar RNA (snoRNA) SNORD116 and non-coding RNA IPW (Imprinted in Prader-Willi) exons. SNORD116 affects the transcription profile of hundreds of genes, possibly via DNA methylation or post-transcriptional modification, although the exact mechanism is not completely clear. IPW on the other hand has been shown to specifically modulate histone methylation of a separate imprinted locus, the DLK1-DIO3 cluster, which itself is associated with several neurodevelopmental disorders with similarities to PWS. Here we review what is currently known of the molecular targets of SNORD116 and IPW and begin to disentangle their roles in contributing to the Prader-Willi Syndrome phenotype. Full article
Show Figures

Figure 1

Back to TopTop