Human DNA replication initiation sites are specified epigenetically by oxidation of 5-methyl-deoxycytidine.

DNA replication initiates at tens of thousands of sites on the human genome during each S phase. However, no consensus DNA sequence has been found that specifies the locations of these replication origins. Here, we investigate modifications of human genomic DNA by density equilibrium centrifugation and DNA sequencing. We identified short discrete sites with increased density during quiescence and G1 phase that overlap with DNA replication origins before their activation in S phase. The increased density is due to the oxidation of 5-methyl-deoxycytidines by ten-eleven-translocation DNA dioxygenase (TET) enzymes at GC-rich domains. Reversible inhibition of de novo methylation and of subsequent oxidation of deoxycytidines results in a reversible inhibition of DNA replication and of cell proliferation. Our findings suggest a mechanism for the epigenetic specification and semiconservative inheritance of DNA replication origin sites in human cells that also provides a stable integral DNA replication licence to support once-per-cell cycle control of origin activation.

Publication Details

Journal
The Francis Crick Institute
Published
2025-05-06
DOI
https://doi.org/10.25418/crick.28937798
Primary Topic
Epigenetics and DNA Methylation
Type
article
Field-Weighted Citation Impact
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article

Human DNA replication initiation sites are specified epigenetically by oxidation of 5-methyl-deoxycytidine.

The Francis Crick Institute
Epigenetics and DNA Methylation
article

Human DNA replication initiation sites are specified epigenetically by oxidation of 5-methyl-deoxycytidine.

article en

Abstract

DNA replication initiates at tens of thousands of sites on the human genome during each S phase. However, no consensus DNA sequence has been found that specifies the locations of these replication origins. Here, we investigate modifications of human genomic DNA by density equilibrium centrifugation and DNA sequencing. We identified short discrete sites with increased density during quiescence and G1 phase that overlap with DNA replication origins before their activation in S phase. The increased density is due to the oxidation of 5-methyl-deoxycytidines by ten-eleven-translocation DNA dioxygenase (TET) enzymes at GC-rich domains. Reversible inhibition of de novo methylation and of subsequent oxidation of deoxycytidines results in a reversible inhibition of DNA replication and of cell proliferation. Our findings suggest a mechanism for the epigenetic specification and semiconservative inheritance of DNA replication origin sites in human cells that also provides a stable integral DNA replication licence to support once-per-cell cycle control of origin activation.

The Francis Crick Institute
Openalex Percentile: Top 61%
Epigenetics and DNA Methylation
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Human DNA replication initiation sites are specified epigenetically by oxidation of 5-methyl-deoxycytidine. · The Francis Crick Institute (2025) | TGRS Research Map | TGRS