ArticleMolecular cell2025
Identification of molecular determinants of gene-specific bursting patterns by high-throughput imaging screens.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- Protocol to measure transcriptional bursting of endogenous genes using high-throughput RNA-FISH.STAR protocols · 2026Article
- TAD boundaries and gene activity are uncoupled.eLife · 2026Article
- TAD boundaries and gene activity are uncoupled.bioRxiv : the preprint server for biology · 2026Article
- What makes genes burst.Trends in cell biology · 2026Review
- Timing is everything: transcription bursting in development.Genes & development · 2025Review
- Regulation of RNA polymerase II transcription through re-initiation and bursting.Molecular cell · 2025Review
- Decoding stimulus-specific regulation of promoter activity of p53 target genes.Frontiers in cell and developmental biology · 2025Article
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5 authors.
Funding
Abstract
Stochastic transcriptional bursting is a universal property of active genes. While different genes exhibit distinct bursting patterns, the molecular mechanisms that govern gene-specific stochastic bursting are largely unknown. We have developed a high-throughput-imaging-based screening strategy to identify cellular factors that determine the bursting patterns of native genes in human cells. We identify protein acetylation as a prominent effector of burst frequency and burst size acting via decreasing off-times and gene-specific changes in the on-time. These effects are not correlated with promoter acetylation. Instead, we demonstrate acetylation of the Integrator complex as a key determinant of gene bursting that alters Integrator interactions with transcription elongation and RNA processing factors but without affecting pausing. Our results suggest a prominent role for non-histone acetylation of a transcription cofactors as a mechanism for modulation of bursting via a far-downstream checkpoint.
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