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Cited by 31Psoriasis: Treatment and PathogenesisGenomics and Chromatin DynamicsGenetic Associations and Epidemiology

Mapping DNA interaction landscapes in psoriasis susceptibility loci highlights KLF4 as a target gene in 9q31

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Ray-Jones, Helen, Duffus, Kate, McGovern, Amanda, Martin, Paul, Shi, Chenfu, Hankinson, Jenny, Gough, Oliver, Yarwood, Annie +10 more·2020·BMC Biology
DOI 10.1186/s12915-020-00779-3PMC PMC7199343
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Abstract

Background: Genome-wide association studies (GWAS) have uncovered many genetic risk loci for psoriasis, yet many remain uncharacterised in terms of the causal gene and their biological mechanism in disease. This is largely a result of the findings that over 90% of GWAS variants map outside of protein-coding DNA and instead are enriched in cell type- and stimulation-specific gene regulatory regions. Results: Here, we use a disease-focused Capture Hi-C (CHi-C) experiment to link psoriasis-associated variants with their target genes in psoriasis-relevant cell lines (HaCaT keratinocytes and My-La CD8+ T cells). We confirm previously assigned genes, suggest novel candidates and provide evidence for complexity at psoriasis GWAS loci. For one locus, uniquely, we combine further epigenomic evidence to demonstrate how a psoriasis-associated region forms a functional interaction with the distant (> 500 kb) KLF4 gene. This interaction occurs between the gene and active enhancers in HaCaT cells, but not in My-La cells. We go on to investigate this long-distance interaction further with Cas9 fusion protein-mediated chromatin modification (CRISPR activation) coupled with RNA-seq, demonstrating how activation of the psoriasis-associated enhancer upregulates KLF4 and its downstream targets, relevant to skin cells and apoptosis. Conclusions: This approach utilises multiple functional genomic techniques to follow up GWAS-associated variants implicating relevant cell types and causal genes in each locus; these are vital next steps for the translation of genetic findings into clinical benefit.

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  • 3C-derived methods have detected multitudes of enhancer-promoter loops in many human and mouse cell types.

    “These enrichment methods have detected multitudes of enhancer–promoter loops in many human and mouse cell types [243, 286–291].”

    From Transcriptional enhancers and their communication with gene promoters (2021) · cites this paper as [291]

    The Results section (“Capture Hi-C identified novel gene targets in psoriasis susceptibility loci”; page unavailable) reports an average of 6,593 interactions across three capture experiments in human cell lines, with about 30% involving a transcription start site. The paper also identifies enhancer–promoter interactions using HiChIP in HaCaT cells. It does not establish the claim for many human and mouse cell types; the mouse-cell portion is unsupported by this source. (LLM, conf=0.86)

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Authors
Ray-Jones, H., Duffus, K., McGovern, A., Martin, P., Shi, C., Hankinson, J., Gough, O., Yarwood, A., Morris, A. P., Adamson, A., Taylor, C., Ding, J., Gaddi, V. P., Fu, Y., Gaffney, P., Orozco, G., Warren, R. B., & Eyre, S.
Affiliations
  • Manchester Academic Health Science Centre (GB)
  • University of Manchester (GB)
  • Oklahoma Medical Research Foundation (US)
ORCID
Venue
BMC Biology
Publisher
Springer Science and Business Media LLC
Published
2020-05-04
Volume
18
Issue
1
Pages
47-47
ISSN
1741-7007 (ISSN-L)
DOI
10.1186/s12915-020-00779-3
PMC
PMC7199343
OpenAlex
W3017253057
Cited by
31
References
10
Citations by year
2026: 4 · 2025: 5 · 2024: 4 · 2023: 6 · 2022: 3 · 2021: 6 · 2020: 2 · 2019: 1
FWCI
1.49
Type
journal article
Language
en
Open access
Licence
Locations
  • BMC Biology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Manchester Biomedical Research Centre (N/A)
  • Versus Arthritis (21348 and 21754)
  • Sir Jules Thorn Charitable Trust (PhD scholarship)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords
psoriasis, genetic susceptibility loci, KLF4, long-range chromatin interactions, enhancer-promoter interactions, Capture Hi-C, HaCaT keratinocytes, CD8+ T cells, CRISPR activation, chromatin modification, enhancer activity, causal gene identification, non-coding variants
MeSH terms
HaCaT Cells, Kruppel-Like Factor 4, Chromosome Mapping, DNA, Humans, Psoriasis, Apoptosis, Genetic Predisposition to Disease, Genome-Wide Association Study

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