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Polycomb sustains promoters in a deep OFF-state by limiting PIC formation to counteract transcription

ABSTRACT: Polycomb sustains promoters in a deep OFF-state by limiting PIC formation to counteract transcription

PROVIDER: PRJNA894545 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22054209_1.fastq.gz	Fastqsanger.gz
	SRR22054209_2.fastq.gz	Fastqsanger.gz
	SRR22054210_1.fastq.gz	Fastqsanger.gz
	SRR22054210_2.fastq.gz	Fastqsanger.gz
	SRR22054211_1.fastq.gz	Fastqsanger.gz

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Polycomb sustains promoters in a deep OFF-state by limiting PIC formation to counteract transcription

Project description:The Polycomb system plays fundamental roles in regulating gene expression during mammalian development. However, how it controls transcription to enable gene repression has remained enigmatic. Here we employ rapid degron-based depletion coupled with live-cell transcription imaging and single-particle tracking to uncover how the Polycomb system controls transcription in single cells. We discover that the Polycomb system is not a constitutive block to transcription but instead sustains a long-lived deep promoter OFF-state which limits the frequency with which the promoter can enter into a transcribing state. We demonstrate that Polycomb sustains this deep promoter OFF-state by counteracting the binding of factors that enable early transcription pre-initiation complex formation and show that this is necessary for gene repression. Together these important discoveries provide a new rationale for how the Polycomb system controls transcription and suggests a universal mechanism that could enable the Polycomb system to constrain transcription across diverse cellular contexts.

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Melanoma SK-Mel-103 cell line : control vs. treated with pIC/pIC+PEI

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Foreskin Melanocyte: control vs. treated with pIC/pIC+PEI

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An integrated SAGA and TFIID PIC assembly pathway selective for poised and induced promoters [ChIP-Exo]

Project description:Genome-wide, little is understood about how proteins organize at inducible promoters before and after in-duction, and to what extent inducible and constitutive architectures depend on cofactors. We report that se-quence-specific transcription factors and their tethered cofactors (e.g., SAGA, Mediator, TUP, NuA4, SWI/SNF, RPD3-L) are already bound to promoters prior to induction (“poised”), rather than recruited upon induction, whereas induction recruits the pre-initiation complex (PIC). Through depletion and/or deletion ex-periments we show that SAGA does not function at constitutive promoters, although a SAGA-independent Gcn5 does acetylate +1 nucleosomes there. At poised promoters, SAGA catalyzes +1 nucleosome acetylation but not PIC assembly. At induced promoters, SAGA catalyzes acetylation, deubiquitylation, and PIC assembly. Surprisingly, SAGA mediates induction by creating a PIC that allows TFIID to stably associate, rather than creating a TFIID-independent PIC, as is generally thought. These findings suggest that inducible systems, where present, evolved on top of constitutive systems.

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An integrated SAGA and TFIID PIC assembly pathway selective for poised and induced promoters [RNA-Seq]

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