EXPERIMENT_TITLE: GSM5695767: Jlat 8.4 Hi-C (+TNF-alpha, GFP negative); Homo sapiens; Hi-C
EXPERIMENT_DESIGN_LIBRARY_DESCRIPTOR_LIBRARY_CONSTRUCTION_PROTOC: For Hi-C, cells were fixed with 1% formaldehyde for 10 minutes at room temperture, quenched with 0.2M Glycine for 5 minutes. After fixation and quenching, cells were pelleted, washed 1X with DPBS, pelleted again, and frozen on dry ice. Samples were stored in -80C until further processing. In situ Hi-C was performed accoring to Rao et al. Cell 2014 using the MboI restriction enzyme. Libraries were sequenced on the Novoseq 6000 platform.
STUDY_DESCRIPTOR_STUDY_ABSTRACT: The three-dimensional structure of the genome is a regulator of transcription and cell function; HIV-1 infection can influence host cell function, but the degree to which this is mediated through changes to host chromatin architecture is unclear. We interrogated genome-wide chromatin organization and the structure of chromatin around latently infected HIV-1 integration sites using Hi-C and ATAC-seq and combined these data with RNA transcriptional analysis of the provirus and neighboring genes in HIV-inducible cellular models. We found chromatin interaction networks around integrated HIV-1 are predominantly preserved with respect to uninfected cells, proving the lack of an obligate association between latent integration and major chromatin remodeling. Instead, we find that induction of proviral transcription may lead to local changes in chromatin accessibility downstream from the 3' LTR, demonstrating that HIV-1 can alter local cellular chromatin structure post-integration. Using long-read Nanopore RNA-seq, we interrogated the local host and HIV-1 transcriptomes and observed that 1-5% of HIV-1 transcripts initiated at the 5' LTR promoter extended into the flanking cellular genome, generating chimeric virus-host RNAs. Thus, integration leading to latency (and provirus activation) may not lead to obligate global chromatin rearrangements; we also observed, previously unreported, novel changes in chromatin accessibility during HIV-1 transcription. Overall design: Analysis of Hi-C data in Jurkat T-cells and Jurkat-derived JLat models during TNF-alpha induced reversal of HIV latency.
SAMPLE_TITLE: Jlat 8.4 Hi-C (+TNF-alpha, GFP negative)
SAMPLE_SAMPLE_ATTRIBUTES_SAMPLE_ATTRIBUTE: [{"TAG": "source_name", "VALUE": "Jlat 8.4 cell line"}, {"TAG": "cell line", "VALUE": "Jlat 8.4 cell line"}, {"TAG": "experiment type", "VALUE": "MboI in situ Hi-C"}, {"TAG": "treatment", "VALUE": "TNF-alpha"}]
Pool_Member_@attributes_sample_title: Jlat 8.4 Hi-C (+TNF-alpha, GFP negative)
RUN_SET_RUN_Pool_Member_@attributes_sample_title: Jlat 8.4 Hi-C (+TNF-alpha, GFP negative)
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