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Genome-wide mapping of AP sites, binding of repair proteins and G4 structure formation

ABSTRACT: Genome-wide mapping of AP sites, binding of repair proteins and G4 structure formation

PROVIDER: PRJNA596467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10733800.fastq.gz	Fastqsanger.gz
	SRR10733801.fastq.gz	Fastqsanger.gz
	SRR10733802.fastq.gz	Fastqsanger.gz
	SRR10733803.fastq.gz	Fastqsanger.gz
	SRR10733804.fastq.gz	Fastqsanger.gz

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Genome-wide mapping of AP sites, binding of repair proteins and G4 structure formation

Project description:We demonstrate that there is a genome-wide correlation between endogenous AP site damages, binding of repair proteins APE1, AcAPE1 and AcOGG1 and G4 structure formation.

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Project description:G-quadruplexes (G4s) form throughout the genome and influence important cellular processes, but their deregulation can challenge DNA replication fork progression and threaten genome stability. Here, we demonstrate an unexpected, dual role for the dsDNA translocase HLTF in G4 metabolism. First, we find that HLTF is enriched at G4s in the human genome and suppresses G4 accumulation throughout the cell cycle using its ATPase activity. This function of HLTF affects telomere maintenance by restricting alternative lengthening of telomeres, a process stimulated by G4s. We also show that HLTF and MSH2, a mismatch repair factor that binds G4s, act in independent pathways to suppress G4s and to promote resistance to G4 stabilization. In a second, distinct role, HLTF restrains DNA synthesis upon G4 stabilization by suppressing PrimPol-dependent repriming. Together, the dual functions of HLTF in the G4 response prevent DNA damage and potentially mutagenic replication to safeguard genome stability.

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