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Transcription initiation drives dosage compensation establishment and maintenance in male Drosophila [S2_Chip_HistoneMarks]

ABSTRACT: Dosage compensation (DC) in Drosophila equalizes X chromosome-linked gene expression via the Male-Specific Lethal (MSL) complex, which acetylates histone 4 lysine 16 on the male X-chromosome. How DC is established during early embryogenesis remains obscure, largely due to the difficulty of obtaining sufficient sex-specific material at early embryonic stages. Here, we developed a high-throughput embryo sorting strategy and combined newly synthesized RNA-sequencing and RNA-polymerase II (Pol II) profiling to investigate the mechanisms underlying the onset of DC in vivo. We found that changes in transcription initiation occur prior to detectable differences in transcriptional pausing or elongation and represent the primary determinant of enhanced mRNA output during DC establishment. It had hitherto been unclear whether DC establishment and maintenance exerted similar or distinct effects on transcriptional kinetics. Extending genomewide profiling to S2 cells we uncovered Pol II initiation as a general principle underlying both inception and perpetuation of DC-driven transcriptional upregulation.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE307579 | GEO | 2026/05/28

REPOSITORIES: GEO

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Transcription initiation drives dosage compensation establishment and maintenance in male Drosophila

Project description:Dosage compensation (DC) in Drosophila equalizes X chromosome-linked gene expression via the Male-Specific Lethal (MSL) complex, which acetylates histone 4 lysine 16 on the male X-chromosome. How DC is established during early embryogenesis remains obscure, largely due to the difficulty of obtaining sufficient sex-specific material at early embryonic stages. Here, we developed a high-throughput embryo sorting strategy and combined newly synthesized RNA-sequencing and RNA-polymerase II (Pol II) profiling to investigate the mechanisms underlying the onset of DC in vivo. We found that changes in transcription initiation occur prior to detectable differences in transcriptional pausing or elongation and represent the primary determinant of enhanced mRNA output during DC establishment. It had hitherto been unclear whether DC establishment and maintenance exerted similar or distinct effects on transcriptional kinetics. Extending genomewide profiling to S2 cells we uncovered Pol II initiation as a general principle underlying both inception and perpetuation of DC-driven transcriptional upregulation.

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Transcription initiation drives dosage compensation establishment and maintenance in male Drosophila [Embryo CTD mod mNET-Seq]

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CDK7 kinase activity promotes RNA polymerase II promoter escape by facilitating initiation factor release

Project description:Cyclin-dependent kinase 7 (CDK7), part of the general transcription factor TFIIH, promotes gene transcription by phosphorylating the C-terminal domain of RNA polymerase II (RNA Pol II). Here, we combine rapid CDK7 kinase inhibition with multi-omics analysis to unravel the direct functions of CDK7 in human cells. CDK7 inhibition causes RNA Pol II retention at promoters, leading to decreased RNA Pol II initiation and immediate global downregulation of transcript synthesis. Elongation, termination, and recruitment of co-transcriptional factors are not directly affected. Although RNA Pol II, initiation factors, and Mediator accumulate at promoters, RNA Pol II complexes can also proceed into gene bodies without promoter-proximal pausing while retaining initiation factors and Mediator. Further downstream, RNA Pol II phosphorylation increases and initiation factors and Mediator are released, allowing recruitment of elongation factors and an increase in RNA Pol II elongation velocity. Collectively, CDK7 kinase activity promotes the release of initiation factors and Mediator from RNA Pol II, facilitating RNA Pol II escape from the promoter.

2024-05-31 | PXD037842 | Pride

Structural basis of SNAPc-dependent snRNA transcription intiation by RNA polymerase II

Project description:RNA Polymerase II (Pol II) carries out transcription of both protein-coding and non-coding genes. Whereas Pol II initiation at protein-coding genes has been studied in detail, Pol II initiation at non-coding genes such as small nuclear RNA (snRNA) genes is not understood at the structural level. Here we study Pol II initiation at snRNA gene promoters and show that the snRNA-activating protein complex (SNAPc) enables DNA opening and transcription initiation independent of TFIIE and TFIIH in vitro. We then resolve cryo-EM structures of the SNAPc-containing Pol II preinitiation complex (PIC) assembled on U1 and U5 snRNA promoters. The core of SNAPc binds two turns of DNA and recognizes the snRNA promoter-specific proximal sequence element (PSE) located upstream of the TATA box-binding protein TBP. Two extensions of SNAPc called wing-1 and wing-2 bind TFIIA and TFIIB, respectively, explaining how SNAPc directs Pol II to snRNA promoters. Comparison of structures of closed and open promoter complexes elucidates TFIIH-independent DNA opening. These results provide the structural basis of Pol II initiation at non-coding RNA gene promoters.

2023-03-11 | PXD033638 | Pride

Single-molecule imaging reveals RNA Polymerase II dynamics and TAF1-dependent promoter-proximal pause release

Project description:Transcription initiation is a highly regulated process that determines gene expression outcomes1,2, yet the dynamics and efficiency of individual initiation events in living cells remain poorly understood. Here we combine endogenous tagging of human RNA polymerase II (Pol II) and the TFIID subunit TAF1 with dual-color live-cell single-molecule imaging to quantitatively map Pol II behavior during transcription initiation and early elongation. Using GRID (Genuine Rate Identification) analysis, we resolved four kinetic populations of chromatin-bound Pol II and find that more than 94% of promoter-bound molecules dissociate within tens of seconds, indicating globally inefficient initiation. Kinetic partitioning of Pol II dwell times into promoter-proximal pausing and gene body elongation reveals a global pausing index that is selectively increased by CDK9 inhibition. Single-cell analysis uncovers substantial heterogeneity in initiation efficiency and pausing that is not explained by cell-cycle state. Spatial heatmap analysis identifies recurrent Pol II ‘hotspots’, nuclear regions enriched for repeated long-lived Pol II binding events, whose abundance and architecture are selectively perturbed by inhibitors that trap Pol II at promoters or disrupt TFIID. Finally, acute depletion of TAF1 leaves initiation efficiency unchanged but significantly increases the pausing index and reduces elongation efficiency, consistent with impaired pause release. Together, these findings establish a general framework to quantify transcription efficiency in vivo and support a model in which TAF1, and by extension TFIID, promotes pause release and productive elongation.

2026-06-03 | PXD072625 | Pride

CDK7 kinase activity promotes RNA polymerase II promoter escape by facilitating initiation factor release

Project description:Cyclin-dependent kinase 7 (CDK7), part of general transcription factor TFIIH, promotes gene transcription by phosphorylating the C-terminal domain of RNA polymerase II (Pol II). Here, we combine rapid CDK7 kinase inhibition with multi-omics analysis to unravel the direct functions of CDK7 in human cells. CDK7 inhibition causes Pol II retention at promoters, leading to decreased Pol II initiation and immediate global downregulation of transcript synthesis. Elongation, termination, and recruitment of co-transcriptional factors are not directly affected. Although Pol II, initiation factors, and Mediator accumulate at promoters, Pol II complexes can also proceed into gene bodies without promoter-proximal pausing while retaining initiation factors and Mediator. Further downstream, Pol II phosphorylation increases, initiation factors and Mediator are released, allowing recruitment of elongation factors and increase in Pol II elongation velocity. Collectively, CDK7 kinase activity promotes the release of initiation factors and Mediator from Pol II, facilitating Pol II escape from the promoter.

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