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Oxidative stress triggers RNAPII arrest through PARylation and DNA damage [ChIP-seq]

GSE335230 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 6 samples Submitted 2026/06/12 Platform GPL30173
Summary
UV or gamma irradiation, as well as certain chemicals, generate DNA damage that disrupts transcription through a variety of well-characterised mechanisms. In contrast, the transcriptional response to oxidative stress remains poorly understood. Here, we describe a rapid and widespread shutdown of transcription following oxidative DNA base damage. By monitoring RNAPII occupancy and elongation dynamics, we demonstrate that oxidative stress temporarily halts RNAPII pause release and arrests the progression of elongation complexes within the gene body. We present evidence that this occurs in a unique and transient manner, characterised by abrupt arrest of elongating RNAPII dead in its tracks, followed by rapid transcriptional recovery as DNA lesions are repaired. We find that the restriction of initiation and early elongation complexes is regulated by PARylation, whereas recovery of RNAPII arrested within the gene body requires DNA repair mediated by the base excision repair (BER) and single-strand break repair (SSBR) pathways.
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Direct links to NCBI, no account and no request form: the whole study as GSE335230_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1275866 and SRA study SRP591627. Searching any of these in the dataset finder brings you back here.

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