ArticleProceedings of the National Academy of Sciences of the United States of America2007
Drosophila follicle cell amplicons as models for metazoan DNA replication: a cyclinE mutant exhibits increased replication fork elongation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- In Silico Born Designed Anti-EGFR Aptamer Gol1 Has Anti-Proliferative Potential for Patient Glioblastoma Cells.International journal of molecular sciences · 2025Article
- Finishing the egg.Genetics · 2024Article
- Su(Hw) primes 66D and 7F Drosophila chorion genes loci for amplification through chromatin decondensation.Scientific reports · 2021Article
- DNA Replication Control DuringGenetics · 2017Review
- Multiple mechanisms contribute to double-strand break repair at rereplication forks in Drosophila follicle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Replication fork progression during re-replication requires the DNA damage checkpoint and double-strand break repair.Current biology : CB · 2015Article
- Drosophila embryonic cell-cycle mutants.G3 (Bethesda, Md.) · 2013Article
- Cyclin E controls Drosophila female germline stem cell maintenance independently of its role in proliferation by modulating responsiveness to niche signals.Development (Cambridge, England) · 2013Article
- Developmental control of gene copy number by repression of replication initiation and fork progression.Genome research · 2012Article
- Safeguarding genetic information in Drosophila.Chromosoma · 2011Review
- Integrative analysis of gene amplification in Drosophila follicle cells: parameters of origin activation and repression.Genes & development · 2011Article
- Distinct and redundant functions of cyclin E1 and cyclin E2 in development and cancer.Cell division · 2010Article
- Cyclin E is stabilized in response to replication fork barriers leading to prolonged S phase arrest.The Journal of biological chemistry · 2009Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Gene clusters amplified in the ovarian follicle cells of Drosophila serve as powerful models for metazoan DNA replication. In response to developmental signals, specific genomic regions undergo amplification by repeated firing of replication origins and bidirectional movement of replication forks for approximately 50 kb in each direction. Previous work focused on initiation of amplification, defining replication origins, establishing the role of the prereplication complex and origin recognition complex (ORC), and uncovering regulatory functions for the Myb, E2F1, and Rb transcription factors. Here, we exploit follicle cell amplification to investigate the control of DNA replication fork progression and termination, poorly understood processes in metazoans. We identified a mutant in which, during gene amplification, the replication forks move twice as far from the origin compared with wild type. This phenotype is the result of an amino acid substitution mutation in the cyclinE gene, cyclinE(1f36). The rate of oogenesis is normal in cyclinE(1f36)/cyclinE(Pz8) mutant ovaries, indicating that increased replication fork progression is due to increased replication fork speed, possibly from increased processivity. The increased amplification domains observed in the mutant imply that there are not replication fork barriers preventing replication forks from progressing beyond the normal 100-kb amplified region. These results reveal a previously unrecognized role for CyclinE in controlling replication fork movement.
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