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Jill E Moore

Publications and source records attributed to Jill E Moore.

2 recordsLinked to original sources

An encyclopedia of human enhancer-gene regulatory interactions.

Identifying transcriptional enhancers and their target genes is essential for understanding gene regulation and the effect of human genetic variation on disease1-6. Here we create and evaluate a resource of more than 92 million enhancer-gene regulatory interactions across 1,458 biosamples covering 369 cell types and tissues, by integrating predictive models, chromatin states, three-dimensional contacts and large-scale genetic perturbations generated by the ENCODE Consortium7. We first create a systematic benchmarking pipeline to compare predictive models, assembling a dataset of 10,356 element-gene pairs measured in CRISPR perturbation experiments, more than 30,000 fine-mapped expression quantitative trait loci and 569 fine-mapped genome-wide association study (GWAS) variants linked to a probable causal gene. Using this framework, we develop ENCODE-rE2G, a predictive model achieving state-of-the-art performance across several prediction tasks, demonstrating that iterative perturbations and supervised machine learning can build increasingly accurate predictive models of enhancer regulation. Using ENCODE-rE2G, we build an encyclopedia of enhancer-gene regulatory interactions in the human genome, revealing global properties of enhancer networks, identifying differences in regulatory complexity across genes and improving analyses linking noncoding variants to target genes and cell types for common complex diseases. By interpreting the model, we find that beyond enhancer activity and three-dimensional enhancer-promoter contacts, additional features that guide enhancer-promoter communication include promoter class and enhancer-enhancer synergy. These genome-wide maps of enhancer-gene regulatory interactions, benchmarking software, predictive models and insights about enhancer function provide a valuable resource for future studies of gene regulation and human genetics.

Humans

Identifying independent causal cell types for human diseases and risk variants.

The SNP-heritability of human diseases is extremely enriched in candidate regulatory elements (cREs) from disease-relevant cell types. Critical next steps are to understand whether these enrichments are driven by multiple causal cell types and whether individual variants impact disease risk via a single or multiple of cell types. Here, we propose CT-FM and CT-FM-SNP, 2 methods accounting for cREs shared across cell types to identify independent sets of causal cell types for a trait and its candidate causal variants, respectively. We applied CT-FM to 63 GWAS summary statistics (average N = 417K) using 924 cRE annotations, primarily from ENCODE4. CT-FM inferred 79 sets of causal cell types, with corresponding SNP-annotations explaining 39.0 ± 1.8% of trait SNP-heritability. It identified 14 traits with independent causal cell types, uncovering previously unexplored cellular mechanisms in height, schizophrenia and autoimmune diseases. We applied CT-FM-SNP to 39 UK Biobank traits and predicted high-confidence causal cell types for 3,091 candidate causal non-coding SNPs-trait pairs. Our results suggest that most SNPs affect a phenotype via a single set of cell types, whereas pleiotropic SNPs might target different cell types depending on the phenotype context. Altogether, CT-FM and CT-FM-SNP shed light on how genetic variants act collectively and individually at the cellular level to affect disease risk.

Journal Article