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Parental Origin of Interstitial Duplications at 15q11.2-q13.3 in Schizophrenia and Neurodevelopmental Disorders.

Authors :
Anthony R Isles
Andrés Ingason
Chelsea Lowther
James Walters
Micha Gawlick
Gerald Stöber
Elliott Rees
Joanna Martin
Rosie B Little
Harry Potter
Lyudmila Georgieva
Lucilla Pizzo
Norio Ozaki
Branko Aleksic
Itaru Kushima
Masashi Ikeda
Nakao Iwata
Douglas F Levinson
Pablo V Gejman
Jianxin Shi
Alan R Sanders
Jubao Duan
Joseph Willis
Sanjay Sisodiya
Gregory Costain
Thomas M Werge
Franziska Degenhardt
Ina Giegling
Dan Rujescu
Stefan J Hreidarsson
Evald Saemundsen
Joo Wook Ahn
Caroline Ogilvie
Santhosh D Girirajan
Hreinn Stefansson
Kari Stefansson
Michael C O'Donovan
Michael J Owen
Anne Bassett
George Kirov
Source :
PLoS Genetics, Vol 12, Iss 5, p e1005993 (2016)
Publication Year :
2016
Publisher :
Public Library of Science (PLoS), 2016.

Abstract

Duplications at 15q11.2-q13.3 overlapping the Prader-Willi/Angelman syndrome (PWS/AS) region have been associated with developmental delay (DD), autism spectrum disorder (ASD) and schizophrenia (SZ). Due to presence of imprinted genes within the region, the parental origin of these duplications may be key to the pathogenicity. Duplications of maternal origin are associated with disease, whereas the pathogenicity of paternal ones is unclear. To clarify the role of maternal and paternal duplications, we conducted the largest and most detailed study to date of parental origin of 15q11.2-q13.3 interstitial duplications in DD, ASD and SZ cohorts. We show, for the first time, that paternal duplications lead to an increased risk of developing DD/ASD/multiple congenital anomalies (MCA), but do not appear to increase risk for SZ. The importance of the epigenetic status of 15q11.2-q13.3 duplications was further underlined by analysis of a number of families, in which the duplication was paternally derived in the mother, who was unaffected, whereas her offspring, who inherited a maternally derived duplication, suffered from psychotic illness. Interestingly, the most consistent clinical characteristics of SZ patients with 15q11.2-q13.3 duplications were learning or developmental problems, found in 76% of carriers. Despite their lower pathogenicity, paternal duplications are less frequent in the general population with a general population prevalence of 0.0033% compared to 0.0069% for maternal duplications. This may be due to lower fecundity of male carriers and differential survival of embryos, something echoed in the findings that both types of duplications are de novo in just over 50% of cases. Isodicentric chromosome 15 (idic15) or interstitial triplications were not observed in SZ patients or in controls. Overall, this study refines the distinct roles of maternal and paternal interstitial duplications at 15q11.2-q13.3, underlining the critical importance of maternally expressed imprinted genes in the contribution of Copy Number Variants (CNVs) at this interval to the incidence of psychotic illness. This work will have tangible benefits for patients with 15q11.2-q13.3 duplications by aiding genetic counseling.

Subjects

Subjects :
Genetics
QH426-470

Details

Language :
English
ISSN :
15537390 and 15537404
Volume :
12
Issue :
5
Database :
Directory of Open Access Journals
Journal :
PLoS Genetics
Publication Type :
Academic Journal
Accession number :
edsdoj.f2c482f1697e4b449a6646761c46db4e
Document Type :
article
Full Text :
https://doi.org/10.1371/journal.pgen.1005993