Genome-wide analysis of primary microRNA expression using H3K36me3 ChIP-seq data

Abstract

Graphical abstract

Cell-type-specific characterization of miRNA gene dynamics in immune cell subpopulations during aging and atherosclerosis disease development at single-cell resolution

“…This could benefit the characterization of differences in alternative transcripts within miRNA gene loci. However, if strand specificity is lacking, this analysis has similar limitations as chromatin immunoprecipitation (ChIP)-seq based analysis of transcriptional activity, described in 10 . In both platforms, the detection of miRNA gene transcription suffers from limited number of intronic reads captured.…”

“…Acknowledging that single-cell transcriptomics captures between 17 to 23% of unspliced reads 8 , analysis of pri-miRNA transcripts presents an alternative. In our previous work, we developed a comprehensive miRNA gene annotation approach based on nascent transcriptome (Global-run-on coupled with sequencing, GRO-seq), Cap Analysis of Gene Expression (CAGE) and histone marker data that enabled the quantification of pri-miRNA transcriptional activity in a multitude of bulk genomics studies in cell lines and primary tissue contexts 9,10 .…”

Predicting the Effect of miRNA on Gene Regulation to Foster Translational Multiomics Research – A Thorough Review on the Role of ChIP-Seq Data

“…Whyte et al [6] SEs play key roles in the control of mammalian cell identity; formation of SE driven feedback loops; regulation of SE-associated gene expression via master TFs Hnisz et al [7] SEs are occupied more frequently by terminal TFs of the Wnt, TGF-b, and LIF signaling pathways in ESCs/cancer cells; and SE-driven genes respond to manipulation of these pathways compared to typical enhancers Hnisz et al [10] Cancer cells generate SE at oncogenes and other genes related to tumor pathogenesis Lovén et al [14] SEs are associated with critical oncogenic drivers in cancer cells Suzuki et al [45,56] SEs potentially drive the biogenesis of miRNAs crucial for cell identity via enhancement of both transcription and Drosha/DGCR8-mediated primary miRNA processing Ri et al [47] Over-expression of miR-1301 induced by deletion of KLF6 SE inhibits cell proliferation in HepG2 cells Liang et al [57] SE-TF regulatory network plays a crucial role in the carcinogenesis of malignant tumour Javierre et al [62] Promoter interactions are highly cell-type specific and enriched for association between active promoters and epigenetically marked enhancers Hu et al [63] IKAROS, prominently associated with leukemia, collaborates with TFs and SEs via FFL, and triggers aberrant gene expression program in a B-cell epithelial transition Zhou et al [65] SE-driven TF gene mediates oncogenesis in Natural Killer/T Cell Lymphoma Scholz et al [73] WNT signaling activates MYC expression via SE in cancer cells Zhang et al [78] miRNAs driven by SEs positively regulate Hippo pathway during liver development Das et al [79] miRNAs driven by SEs mediates immune-suppression Tan et al [80] miRNAs/genes with positive correlations tend to form super-enhancer-like regions Turunen et al [81] Synergistic role of miRNAs and TFs on SEs associated with Hippo signaling pathway…”

A computational modeling of pri-miRNA expression

“…This scarcity is largely because rarely are the pri-miRNAs known, especially their transcriptional start sites (TSSs) [29]. The TSS of a miRNA gene can be tens or hundreds of thousand base pairs away from the location of the precursor and mature miRNAs [29][30][31][32][33]. Despite over a decade of computational and experimental identification of pri-miRNA TSSs and several collections of pri-miRNA TSS annotation through high-throughput experimental studies, the annotated pri-miRNA TSSs were not consistent across studies [29,31,32].…”