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Effect of specific G-quadruplex stabilization on gene expression and chromatin accessibility at gene promoters in Hela cells.

ABSTRACT: Effect of specific G-quadruplex stabilization on gene expression and chromatin accessibility at gene promoters in Hela cells.

PROVIDER: PRJNA1075785 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27955610_1.fastq.gz	Fastqsanger.gz
	SRR27955610_2.fastq.gz	Fastqsanger.gz
	SRR27955611_1.fastq.gz	Fastqsanger.gz
	SRR27955611_2.fastq.gz	Fastqsanger.gz
	SRR27955612_1.fastq.gz	Fastqsanger.gz

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Effect of specific G-quadruplex stabilization on gene expression and chromatin accessibility at gene promoters in Hela cells.

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Project description:G-quadruplexes (G4s) are noncanonical DNA secondary structures formed through the self-association of guanines. They are distributed genome-widely and participate in multiple biological processes including gene transcription, and quadruplex-targeted ligands serve as potential therapeutic agents for DNA-targeted therapies. However, the roles of G-quadruplexes in transcriptional regulation remains elusive. Here, we establish a sensitive G4-CUT&Tag method for genome-wide profiling of native G-quadruplexes with high resolution and specificity. We find that native G-quadruplex signals are cell-type specific and are associated with transcriptional regulatory elements with active epigenetic modifications. Promoter-proximal RNA polymerase II pausing promotes native G-quadruplex formation, oppositely, G-quadruplex stabilization by quadruplex-targeted ligands globally reduces RNA polymerase II occupancy at gene promoters as well as nascent RNA synthesis. Moreover, G-quadruplex stabilization modulates chromatin states and impedes transcription initiation via inhibiting the loading of general transcription factors to promoters.Together, these studies reveal a reciprocal regulation between native G-quadruplex dynamics and gene transcription in the genome, which will deepen our knowledge of G-quadruplex biology towards considering therapeutically targeting G-quadruplexes in human diseases.

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