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Exploring the overlap between rheumatoid arthritis susceptibility loci and long non-coding RNA annotations
James Ding1, Chenfu Shi1, John Bowes1,2
1Division of Musculoskeletal and Dermatological Sciences, Centre for Genetics and Genomics Versus Arthritis, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, England, United Kingdom.
Plos One
|March 21, 2020
Summary
Genetic variants linked to rheumatoid arthritis (RA) risk may not directly disrupt long non-coding RNAs (lncRNAs). Instead, immune-relevant enhancers are enriched among RA susceptibility variants, suggesting a different disease mechanism.
Area of Science:
- Genetics
- Immunology
- Molecular Biology
Background:
- Susceptibility variants for complex diseases like rheumatoid arthritis (RA) are known, but the mechanisms of risk mediation remain unclear.
- Many risk variants are non-coding, and long non-coding RNAs (lncRNAs) are found to be enriched in variants associated with RA and other complex diseases.
Purpose of the Study:
- To investigate the extent to which direct disruption of lncRNAs might mediate RA susceptibility.
- To determine if lncRNA disruption, independent of enhancer disruption, plays a significant role in complex disease susceptibility.
Main Methods:
- Utilized annotated features to model disease susceptibility.
- Tested for enrichment of enhancers and immune-enriched lncRNAs among RA susceptibility variants.
- Conditioned models on immune-relevant enhancers to assess independent effects of lncRNAs.
Main Results:
- Demonstrated significant local enrichment of enhancers from immune-relevant cell types among RA susceptibility variants (log2 enrichment 3.40).
- Observed a small but significant enrichment for immune-enriched lncRNAs (log2 enrichment 0.867), which disappeared when conditioned on enhancers (log2 enrichment -0.37).
- Found that immune-enriched lncRNAs are expressed at low levels, potentially limiting functional characterization.
Conclusions:
- Direct disruption of lncRNA sequence, independent of enhancer disruption, does not appear to be a major mechanism for RA susceptibility.
- Immune-relevant enhancers are more strongly associated with RA risk variants than lncRNAs.
- Low expression levels of immune-enriched lncRNAs may hinder functional studies and mechanistic understanding.
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