ArticleNucleic acids research2011
A distinct first replication cycle of DNA introduced in mammalian cells.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- The telomerase reverse transcriptase elongates reversed replication forks at telomeric repeats.Science advances · 2023Article
- Article
- Genome-wide Identification of Structure-Forming Repeats as Principal Sites of Fork Collapse upon ATR Inhibition.Molecular cell · 2018Article
- MutSβ abundance and Msh3 ATP hydrolysis activity are important drivers of CTG•CAG repeat expansions.Nucleic acids research · 2017Article
- Activation of a human chromosomal replication origin by protein tethering.Nucleic acids research · 2013Article
- Mature microsatellites: mechanisms underlying dinucleotide microsatellite mutational biases in human cells.G3 (Bethesda, Md.) · 2013Article
- Complexes between two GAA Repeats within DNA introduced into Cos-1 cells.Mobile genetic elements · 2012Article
- Effects of Friedreich's ataxia GAA repeats on DNA replication in mammalian cells.Nucleic acids research · 2012Article
- Article
- Getting to the core of repeat expansions by cell reprogramming.Cell stem cell · 2010Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many mutation events in microsatellite DNA sequences were traced to the first embryonic divisions. It was not known what makes the first replication cycles of embryonic DNA different from subsequent replication cycles. Here we demonstrate that an unusual replication mode is involved in the first cycle of replication of DNA introduced in mammalian cells. This alternative replication starts at random positions, and occurs before the chromatin is fully assembled. It is detected in various cell lines and primary cells. The presence of single-stranded regions increases the efficiency of this alternative replication mode. The alternative replication cannot progress through the A/T-rich FRA16B fragile site, while the regular replication mode is not affected by it. A/T-rich microsatellites are associated with the majority of chromosomal breakpoints in cancer. We suggest that the alternative replication mode may be initiated at the regions with immature chromatin structure in embryonic and cancer cells resulting in increased genomic instability. This work demonstrates, for the first time, differences in the replication progression during the first and subsequent replication cycles in mammalian cells.
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