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The role of LEDGF in transcription is exploited by HIV-1 to position integration

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE279688 | GEO | 2026/02/25

REPOSITORIES: GEO

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The role of LEDGF in transcription is exploited by HIV-1 to position integration [RNA]

Project description:HIV-1 integration occurs across actively transcribed genes due to the interaction of integrase with chromatin factor LEDGF. Although LEDGF was originally purified as a co-activator that stimulates promoters, this role is inconsistent with LEDGF-mediated integration across gene bodies and with data indicating LEDGF promotes transcriptional elongation. We found LEDGF is enriched primarily at transcription start sites (TSSs) of active promoters. Additional data shows MLL1 recruits LEDGF to promoters and LEDGF recruits RNA Pol II. Contrary to existing models, we find that integration into genes is independent of interactions between H3K36me3 and the PWWP domain of LEDGF. Instead, it is the level of LEDGF at TSSs that determines gene specificity of integration. These data support a dual role model of LEDGF where it is tethered to promoters by MLL1 and recruits RNA Pol II. Subsequently, LEDGF travels across the sequences of genes to effect HIV-1 integration.

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The role of LEDGF in transcription is exploited by HIV-1 to position integration

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Project description:Disruption of HIV-1 Integrase (IN) interactions with the host-factor Lens Epithelium-Derived Growth Factor (LEDGF)/p75 leads to decreased, random integration, increased latent infection, and described here, accumulation of HIV-1 antisense RNA (asRNA). asRNA increase was observed following interruptions of IN-LEDGF/p75 interactions either through pharmacologic perturbations of IN-LEDGF/p75 by treatment with allosteric HIV-1 integrase inhibitors (ALLINIs) or in cell lines with LEDGF genetic knockout. Additionally, by impairing Tat-dependent HIV transcription, asRNA abundance markedly increases. Illumina sequencing characterization of asRNA transcripts in primary T cells infected in the presence of ALLINIs showed that most initiate from within the HIV-1. Overall, loss of IN-LEDGF/p75 interactions increase asRNA abundance. Understanding the relationship between ALLINIs, integration sites, asRNA, and latency could aid in future therapeutic strategies.

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