dc.contributor.author |
Fadason, Tayaza |
en |
dc.contributor.author |
Schierding, William |
en |
dc.contributor.author |
Lumley, Thomas |
en |
dc.contributor.author |
O'Sullivan, Justin |
en |
dc.date.accessioned |
2019-03-20T04:12:54Z |
en |
dc.date.issued |
2018-12-05 |
en |
dc.identifier.citation |
Nature communications 9(1):5198 05 Dec 2018 |
en |
dc.identifier.issn |
2041-1723 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/46205 |
en |
dc.description.abstract |
Clinical studies of non-communicable diseases identify multimorbidities that suggest a common set of predisposing factors. Despite the fact that humans have ~24,000 genes, we do not understand the genetic pathways that contribute to the development of multimorbid non-communicable disease. Here we create a multimorbidity atlas of traits based on pleiotropy of spatially regulated genes. Using chromatin interaction and expression Quantitative Trait Loci (eQTL) data, we analyse 20,782 variants (p < 5 × 10-6) associated with 1351 phenotypes to identify 16,248 putative spatial eQTL-eGene pairs that are involved in 76,013 short- and long-range regulatory interactions (FDR < 0.05) in different human tissues. Convex biclustering of spatial eGenes that are shared among phenotypes identifies complex interrelationships between nominally different phenotype-associated SNPs. Our approach enables the simultaneous elucidation of variant interactions with target genes that are drivers of multimorbidity, and those that contribute to unique phenotype associated characteristics. |
en |
dc.format.medium |
Electronic |
en |
dc.language |
eng |
en |
dc.relation.ispartofseries |
Nature communications |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.rights.uri |
http://creativecommons.org/licenses/by/4.0/ |
en |
dc.subject |
Chromatin |
en |
dc.subject |
Humans |
en |
dc.subject |
Disease |
en |
dc.subject |
Phenotype |
en |
dc.subject |
Polymorphism, Single Nucleotide |
en |
dc.subject |
Quantitative Trait Loci |
en |
dc.subject |
Genome, Human |
en |
dc.subject |
Genome-Wide Association Study |
en |
dc.subject |
Multimorbidity |
en |
dc.title |
Chromatin interactions and expression quantitative trait loci reveal genetic drivers of multimorbidities. |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1038/s41467-018-07692-y |
en |
pubs.issue |
1 |
en |
pubs.begin-page |
5198 |
en |
pubs.volume |
9 |
en |
dc.rights.holder |
Copyright: The authors |
en |
pubs.publication-status |
Published |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/OpenAccess |
en |
pubs.subtype |
Research Support, Non-U.S. Gov't |
en |
pubs.subtype |
research-article |
en |
pubs.subtype |
Journal Article |
en |
pubs.elements-id |
757903 |
en |
pubs.org-id |
Liggins Institute |
en |
pubs.org-id |
Science |
en |
pubs.org-id |
Statistics |
en |
dc.identifier.eissn |
2041-1723 |
en |
pubs.record-created-at-source-date |
2018-12-07 |
en |
pubs.dimensions-id |
30518762 |
en |