Motivation: HiChIP is a powerful tool to interrogate 3D chromatin organization. Current tools to analyse chromatin looping mechanisms using HiChIP data require the identification of loop anchors to work properly. However, current approaches to discover these anchors from HiChIP data are not satisfactory, having either a very high false discovery rate or strong dependence on sequencing depth. Moreover, these tools do not allow quantitative comparison of peaks across different samples, failing to fully exploit the information available from HiChIP datasets.
Results: We develop a new tool based on a representation of HiChIP data centred on the re-ligation sites to identify peaks from HiChIP datasets, which can subsequently be used in other tools for loop discovery. This increases the reliability of these tools and improves recall rate as sequencing depth is reduced. We also provide a method to count reads mapping to peaks across samples, which can be used for differential peak analysis using HiChIP data.
Availability And Implementation: HiChIP-Peaks is freely available at https://github.com/ChenfuShi/HiChIP_peaks.
Supplementary Information: Supplementary data are available at Bioinformatics online.
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http://dx.doi.org/10.1093/bioinformatics/btaa202 | DOI Listing |
Mol Med
November 2024
Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, 510080, China.
Background: Polycomb proteins are conventionally known as global repressors in cell fate determination. However, recent observations have shown their involvement in transcriptional activation, the mechanisms of which need further investigation.
Methods: Herein, multiple data from ChIP-seq, RNA-seq and HiChIP before or after RYBP depletion in embryonic stem cell (ESC), epidermal progenitor (EPC) and mesodermal cell (MEC) were analyzed.
Nucleic Acids Res
November 2024
Department of Pharmacology, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Genome Res
October 2024
State Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai 200438, China;
As a major type of structural variants, tandem duplication plays a critical role in tumorigenesis by increasing oncogene dosage. Recent work has revealed that noncoding enhancers are also affected by duplications leading to the activation of oncogenes that are inside or outside of the duplicated regions. However, the prevalence of enhancer duplication and the identity of their target genes remains largely unknown in the cancer genome.
View Article and Find Full Text PDFMethods Mol Biol
September 2024
Obstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China.
Peakachu is a supervised-learning-based approach that identifies chromatin loops from chromatin contact data. Here, we present Peakachu version 2, an updated version that significantly improves extensibility, usability, and computational efficiency compared to its predecessor. It features pretrained models tailored for a wide range of experimental platforms, such as Hi-C, Micro-C, ChIA-PET, HiChIP, HiCAR, and TrAC-loop.
View Article and Find Full Text PDFNat Commun
July 2024
Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
Cancer genomes are composed of many complex structural alterations on chromosomes and extrachromosomal DNA (ecDNA), making it difficult to identify non-coding enhancer regions that are hijacked to activate oncogene expression. Here, we describe a 3D genomics-based analysis called HAPI (Highly Active Promoter Interactions) to characterize enhancer hijacking. HAPI analysis of HiChIP data from 34 cancer cell lines identified enhancer hijacking events that activate both known and potentially novel oncogenes such as MYC, CCND1, ETV1, CRKL, and ID4.
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