ArticleNucleic acids research2025
Maf1 cooperates with progesterone receptor to repress RNA polymerase III transcription of select tRNAs.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
- An RNA polymerase III tissue and tumor atlas uncovers context-specific activities linked to 3D epigenome regulatory mechanisms.bioRxiv : the preprint server for biology · 2025Article
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9 authors.
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Abstract
Progesterone receptors (PRs) can regulate transcription by RNA polymerase III (Pol III), which transcribes small non-coding RNAs, including all transfer RNAs (tRNAs). We previously demonstrated that PR is associated with the Pol III complex at tRNA genes and that progestins downregulate tRNA transcripts in breast tumor models. To define this mechanism, we investigated the interplay between PR, the Pol III repressor Maf1, and TFIIIB, a core transcription component. ChIP-seq was performed for PR, the Pol III subunits POLR3A, POLR3C, and POLR3G, the TFIIIB component Brf1, and Maf1 in breast cancer cells with or without progestin treatment. With progestin treatment, PR localized to ∼50% of POLR3A-occupied tRNA genes, with Maf1 co-recruited at many of these sites. Progestin treatment did not significantly alter the number of tRNA genes occupied by Pol III subunits or Brf1; however, Brf1 occupancy was stabilized. Progestins downregulated nascent transcription of one-third of tRNA genes; this repression was attenuated by Maf1 knockdown, indicating that Maf1 is required. The PR and Maf1 interaction was also detected by co-immunoprecipitation in a progestin-dependent manner. Overall, these findings demonstrate a ligand-dependent PR-mediated repression of tRNA transcription that involves Maf1.
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