ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/076/SRR19256976/SRR19256976_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/075/SRR19256975/SRR19256975_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/076/SRR19256976/SRR19256976_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/075/SRR19256975/SRR19256975_2.fastq.gzprimaryOK200GenomicsMicrobial Pathogenesis, Yale Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA839152Homo sapiensIn order to identify novel factors associated with regulation of HIV-1 transcription, we completed a genome-wide CRISPRi screen in a monogenic model of HIV-1. We identified SLTM mediated suppression of HIV-1 transcription. We hypothesized that SLTM would alter the chromatin acessibility at the site of HIV-1 integration. We conducted ATAC-seq of CRISPR ready cells encoding a single HIV-1 provirus in the SPECC1 gene transduced with a gRNA targetting SLTM and a Non-Targeting gRNA. We found that SLTM knockdown increased HIV-1 proviral acessibility across the provirus and host acessibility downstream of the site of HIV-1 integration. Overall design: We conducted ATAC-seq of a monogenic Jurkat line with HIV-1 integrated into SPECC1. This line stably expresses dCas9-KRAB and nontargetting and SLTM guide RNAs.ENAfalseATAC-seq of SLTM knockdown in HIV infected JurkatsATAC-seq of SLTM knockdown in HIV infected Jurkats2025-09-242022-05-21PRJNA839152GSE2032359606