ArticleMolecular and cellular biology2000
Replication delay along FRA7H, a common fragile site on human chromosome 7, leads to chromosomal instability.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 112 citations in OpenAlex.
- Frequency and Distribution of Incidental Chromosomal Abnormalities Detected by Peripheral Blood Karyotyping: A Retrospective Study.Genetics research · 2026Article
- Article
- Epigenomic signatures associated with spontaneous and replication stress-induced DNA double strand breaks.Frontiers in genetics · 2022Article
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- New Era of Mapping and Understanding Common Fragile Sites: An Updated Review on Origin of Chromosome Fragility.Frontiers in genetics · 2022Review
- Transcription-Replication Collisions and Chromosome Fragility.Frontiers in genetics · 2021Review
- Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.Cell research · 2020Article
- Article
- Impaired Replication Timing Promotes Tissue-Specific Expression of Common Fragile Sites.Genes · 2020Article
- Review
- Common fragile sites: protection and repair.Cell & bioscience · 2020Review
- Perturbations in the Replication Program Contribute to Genomic Instability in Cancer.International journal of molecular sciences · 2017Review
- Fragility Extraordinaire: Unsolved Mysteries of Chromosome Fragile Sites.Advances in experimental medicine and biology · 2017Review
- Break-seq reveals hydroxyurea-induced chromosome fragility as a result of unscheduled conflict between DNA replication and transcription.Genome research · 2015Article
- Interplay between genetic and epigenetic factors governs common fragile site instability in cancer.Cellular and molecular life sciences : CMLS · 2014Review
- Molecular characterization of common fragile sites as a strategy to discover cancer susceptibility genes.Cellular and molecular life sciences : CMLS · 2014Review
- Genome instability at common fragile sites: searching for the cause of their instability.BioMed research international · 2013Review
- Article
- Sites of genetic instability in mitosis and cancer.Annals of the New York Academy of Sciences · 2012Article
- A genome-wide analysis of common fragile sites: what features determine chromosomal instability in the human genome?Genome research · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites are specific chromosomal loci that show gaps, breaks, or rearrangements in metaphase chromosomes under conditions that interfere with DNA replication. The mechanism underlying the chromosomal instability at fragile sites was hypothesized to associate with late replication time. Here, we aimed to investigate the replication pattern of the common fragile site FRA7H, encompassing 160 kb on the long arm of human chromosome 7. Using in situ hybridization on interphase nuclei, we revealed that the replication of this region is initiated relatively early, before 30% of S phase is completed. However, a high fraction ( approximately 35%) of S-phase nuclei showed allelic asynchrony, indicating that the replication of FRA7H is accomplished at different times in S phase. This allelic asynchrony is not the result of a specific replication time of each FRA7H allele. Analysis of the replication pattern of adjacent clones along FRA7H by using cell population and two-color fluorescent in situ hybridization analyses showed significant differences in the replication of adjacent clones, under normal growth condition and upon aphidicolin treatment. This pattern significantly differed from that of two nonfragile regions which showed a coordinated replication under both conditions. These results indicate that aphidicolin is enhancing an already existing difference in the replication time along the FRA7H region. Based on our replication analysis of FRA7H and on previous analysis of the common fragile site FRA3B, we suggest that delayed replication is underlying the fragility at aphidicolin-induced common fragile sites.
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