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© Research
Publication : Nature communications

Stochastic pausing at latent HIV-1 promoters generates transcriptional bursting.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature communications - 23 Jul 2021

Tantale K, Garcia-Oliver E, Robert MC, L'Hostis A, Yang Y, Tsanov N, Topno R, Gostan T, Kozulic-Pirher A, Basu-Shrivastava M, Mukherjee K, Slaninova V, Andrau JC, Mueller F, Basyuk E, Radulescu O, Bertrand E,

Link to Pubmed [PMID] – 34301927

Link to DOI – 10.1038/s41467-021-24462-5

Nat Commun 2021 07; 12(1): 4503

Promoter-proximal pausing of RNA polymerase II is a key process regulating gene expression. In latent HIV-1 cells, it prevents viral transcription and is essential for latency maintenance, while in acutely infected cells the viral factor Tat releases paused polymerase to induce viral expression. Pausing is fundamental for HIV-1, but how it contributes to bursting and stochastic viral reactivation is unclear. Here, we performed single molecule imaging of HIV-1 transcription. We developed a quantitative analysis method that manages multiple time scales from seconds to days and that rapidly fits many models of promoter dynamics. We found that RNA polymerases enter a long-lived pause at latent HIV-1 promoters (>20 minutes), thereby effectively limiting viral transcription. Surprisingly and in contrast to current models, pausing appears stochastic and not obligatory, with only a small fraction of the polymerases undergoing long-lived pausing in absence of Tat. One consequence of stochastic pausing is that HIV-1 transcription occurs in bursts in latent cells, thereby facilitating latency exit and providing a rationale for the stochasticity of viral rebounds.

https://pubmed.ncbi.nlm.nih.gov/34301927