Noncoding Transcription Is a Driving Force for Nucleosome Instability in <i>spt16</i> Mutant Cells

Feng, Jianxun; Gan, Haiyun; Eaton, Matthew L.; Zhou, Hui; Li, Shuqi; Belsky, Jason A.; MacAlpine, David M.; Zhang, Zhiguo; Li, Qing

doi:10.1128/mcb.00152-16

Cited by 42 publications

(64 citation statements)

References 70 publications

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“…Consistently, reduced nucleosome coverage within transcription units has previously been reported in human and yeast FACT mutants (Carvalho et al, 2013;van Bakel et al, 2013). Nucleosome Depleted Regions (NDRs) are associated with TSSs at gene promoters and may trigger firing from cryptic intragenic TSSs observed by us and others (Carvalho et al, 2013;Feng et al, 2016;Kaplan et al, 2003). However, we find no predisposition in wild type for relaxed chromatin packaging at exonic regions that function as TSSs in FACT mutants (Fig.…”

Section: Discussionsupporting

confidence: 91%

Transcription-driven Chromatin Repression of Intragenic Promoters

Nielsen

Ard

Leng

et al. 2018

Preprint

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Summary:Progression of RNA polymerase II (RNAPII) transcription relies on the appropriately positioned activities of elongation factors. The resulting profile of factors and chromatin signatures along transcription units provides a "positional information system" for transcribing RNAPII. Here, we investigate a chromatin-based mechanism that suppresses intragenic initiation of RNAPII transcription. We demonstrate that RNAPII transcription across gene promoters represses their function in plants. This repression is characterized by reduced promoter-specific molecular signatures and increased molecular signatures associated with RNAPII elongation. The FACT histone chaperone complex is required for this repression mechanism. Genome-wide mapping of Transcription Start Sites (TSSs) reveals thousands of discrete intragenic TSS positions in FACT mutants. Histone 3 lysine 4 mono-methylation poises exonic sites to initiate RNAPII transcription in FACT mutants. Uncovering the mechanism for intragenic TSS repression through the act of RNAPII elongation has important implications for understanding pervasive RNAPII transcription and the regulation of transcript isoform diversity.All rights reserved. No reuse allowed without permission.was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.

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Section: Discussionsupporting

confidence: 91%

Transcription-driven Chromatin Repression of Intragenic Promoters

Nielsen

Ard

Leng

et al. 2018

Preprint

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“…Because the acidic patch binds to many factors, the alterations in nucleosome occupancy and positioning detected in the H2A-E57A mutant are likely the net result of losing multiple interactions. However, we note that a genome-wide reduction in nucleosome occupancy has been reported for an spt16 mutant and for an H2B mutant that lacks the site of ubiquitylation (H2B K123A) (19,94,95). It is also possible that the H2A-E57A substitution intrinsically renders the nucleosome unstable.…”

Section: Discussionmentioning

confidence: 69%

The nucleosome acidic patch directly interacts with subunits of the Paf1 and FACT complexes and controls chromatin architecture in vivo

Cucinotta

Hildreth²,

McShane³

et al. 2019

Preprint

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The nucleosome core regulates DNA-templated processes through the highly conserved nucleosome acidic patch. While structural and biochemical studies have shown that the acidic patch controls chromatin factor binding and activity, few studies have elucidated its functions in vivo. We employed site-specific crosslinking to identify proteins that directly bind the acidic patch in Saccharomyces cerevisiae and demonstrated crosslinking of histone H2A to Paf1 complex subunit Rtf1 and FACT subunit Spt16. Rtf1 bound to nucleosomes through its histone modification domain, supporting its role as a cofactor in H2B K123 ubiquitylation. An acidic patch mutant showed defects in nucleosome positioning and occupancy genome-wide. Our results provide new information on the chromatin engagement of two central players in transcription elongation and emphasize the importance of the nucleosome core as a hub for proteins that regulate chromatin during transcription.Cucinotta et al.

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“…2016) were downloaded from SRA project SRP073244. Spt16 ChlP-seq datasets were downloaded from SRA projects SRP055441 (F eng et al . 2016), SRP018874 (F oltman et al .…”

Section: Methodsmentioning

confidence: 99%

Transcription promotes the interaction of the FAcilitates Chromatin Transactions (FACT) complex with nucleosomes inS. cerevisiae

Howe

Martin

Chruscicki

2018

Preprint

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1The FACT (FAcilitates Chromatin Transactions) complex is enriched on highly 2 expressed genes, where it facilitates transcription while maintaining chromatin structure. 3How it is targeted to these regions is unknown. In vitro, FACT binds destabilized 4 nucleosomes, supporting the hypothesis that FACT is targeted to transcribed chromatin 5 through recognition of RNA polymerase-disrupted nucleosomes. In this study, we used 6 high resolution analysis of FACT occupancy in S. cerevisiae to test this hypothesis. We 7 demonstrate that FACT interacts with unstable nucleosomes in vivo and its interaction 8 with chromatin is dependent on transcription by any of the three RNA polymerases. Deep 9 sequencing of micrococcal nuclease-resistant fragments shows that FACT-bound 10 nucleosomes exhibit differences in micrococcal nuclease sensitivity compared to bulk 11 chromatin, consistent with a modified nucleosome structure being the preferred ligand for 12 this complex. While the presence of altered nucleosomes associated with FACT can also 13 be explained by the known ability of this complex to modulate nucleosome structure, 14 transcription inhibition alleviates this effect indicating that it is not due to FACT 15 interaction alone. Collectively these results suggest that FACT is targeted to transcribed 16 genes through preferential interaction with RNA polymerase disrupted nucleosomes.

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Noncoding Transcription Is a Driving Force for Nucleosome Instability in spt16 Mutant Cells

Cited by 42 publications

References 70 publications

Transcription-driven Chromatin Repression of Intragenic Promoters

Transcription-driven Chromatin Repression of Intragenic Promoters

The nucleosome acidic patch directly interacts with subunits of the Paf1 and FACT complexes and controls chromatin architecture in vivo

Transcription promotes the interaction of the FAcilitates Chromatin Transactions (FACT) complex with nucleosomes inS. cerevisiae

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