Special Issue "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)

Special Issue Editors

Guest Editor
Dr. Florian M. Pauler

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

The University of Vienna, Vienna, Austria
Website | E-Mail
Interests: lncRNAs; epigenetics; transcriptional control; embryology; genomic imprinting; sex determination

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 papers will be 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) is waived for well-prepared manuscripts submitted to this issue. 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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Review

Open AccessReview The Role of the Prader-Willi Syndrome Critical Interval for Epigenetic Regulation, Transcription and Phenotype
Received: 30 July 2018 / Revised: 10 October 2018 / Accepted: 12 October 2018 / Published: 18 October 2018
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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
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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
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