GRaNIE and GRaNPA: inference and evaluation of enhancer‐mediated gene regulatory networks

Aryan Kamal(Heidelberg University), Christian Arnold(European Molecular Biology Laboratory), Annique Claringbould(European Molecular Biology Laboratory), Rim Moussa(European Molecular Biology Laboratory), Nila H. Servaas(European Molecular Biology Laboratory), Maksim Kholmatov(European Molecular Biology Laboratory), N. Daga(European Molecular Biology Laboratory), Daria Nogina(European Molecular Biology Laboratory), Sophia Müller‐Dott(European Molecular Biology Laboratory), Armando Reyes‐Palomares(European Molecular Biology Laboratory), Giovanni Palla(European Molecular Biology Laboratory), Olga Sigalova(Heidelberg University), Daria Bunina(European Molecular Biology Laboratory), Caroline Pabst(Heidelberg University), Judith B. Zaugg(Heidelberg University)
Molecular Systems Biology
April 19, 2023
Cited by 64Open Access
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Abstract

Enhancers play a vital role in gene regulation and are critical in mediating the impact of noncoding genetic variants associated with complex traits. Enhancer activity is a cell-type-specific process regulated by transcription factors (TFs), epigenetic mechanisms and genetic variants. Despite the strong mechanistic link between TFs and enhancers, we currently lack a framework for jointly analysing them in cell-type-specific gene regulatory networks (GRN). Equally important, we lack an unbiased way of assessing the biological significance of inferred GRNs since no complete ground truth exists. To address these gaps, we present GRaNIE (Gene Regulatory Network Inference including Enhancers) and GRaNPA (Gene Regulatory Network Performance Analysis). GRaNIE (https://git.embl.de/grp-zaugg/GRaNIE) builds enhancer-mediated GRNs based on covariation of chromatin accessibility and RNA-seq across samples (e.g. individuals), while GRaNPA (https://git.embl.de/grp-zaugg/GRaNPA) assesses the performance of GRNs for predicting cell-type-specific differential expression. We demonstrate their power by investigating gene regulatory mechanisms underlying the response of macrophages to infection, cancer and common genetic traits including autoimmune diseases. Finally, our methods identify the TF PURA as a putative regulator of pro-inflammatory macrophage polarisation.


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