ArticleDevelopmental cell2016
Proliferation of Double-Strand Break-Resistant Polyploid Cells Requires Drosophila FANCD2.
Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
38 citing papers in PubMed, 49 citations in OpenAlex.
- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Polyploidy and Senescence of Cancer Cells: Impact of Cell Fusion.Advances in experimental medicine and biology · 2026Review
- From survival of irradiated mice to modern molecular insights: a seventy-year journey in radiobiology at the institute of biophysics, Czech academy of sciences.European biophysics journal : EBJ · 2025Review
- Synaptic vesicle glycoprotein 2 enables viable aneuploidy following centrosome amplification.Genetics · 2025Article
- Article
- PLK1 Inhibition Induces Synthetic Lethality in Fanconi Anemia Pathway-Deficient Acute Myeloid Leukemia.Cancer research communications · 2025Article
- Acentric chromosome congression and alignment on the metaphase plate via kinetochore-independent forces.Genetics · 2025Article
- Unusual modes of cell and nuclear divisions characterise Drosophila development.Biochemical Society transactions · 2024Review
- Integrating the Study of Polyploidy Across Organisms, Tissues, and Disease.Annual review of genetics · 2024Review
- The impact of developmental stage, tissue type, and sex on DNA double-strand break repair in Drosophila melanogaster.PLoS genetics · 2024Article
- Broken chromosomes heading into mitosis: More than one way to patch a flat tire.The Journal of cell biology · 2024Review
- The antagonistic relationship between apoptosis and polyploidy in development and cancer.Seminars in cell & developmental biology · 2024Review
- Polyploid Cancer Cell Models in Drosophila.Genes · 2024Review
- Artificial Diploid Escherichia coli by a CRISPR Chromosome-Doubling Technique.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Connections between sister and non-sister telomeres of segregating chromatids maintain euploidy.Current biology : CB · 2023Article
- Conserved function of Drosophila Fancd2 monoubiquitination in response to double-strand DNA breaks.G3 (Bethesda, Md.) · 2022Article
- Polyploidy in development and tumor models in Drosophila.Seminars in cancer biology · 2022Review
- The Cell Biology of Heterochromatin.Cells · 2022Review
- Persistent DNA damage signaling and DNA polymerase theta promote broken chromosome segregation.The Journal of cell biology · 2021Article
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Conserved DNA-damage responses (DDRs) sense genome damage and prevent mitosis of broken chromosomes. How cells lacking DDRs cope with broken chromosomes during mitosis is poorly understood. DDRs are frequently inactivated in cells with extra genomes (polyploidy), suggesting that study of polyploidy can reveal how cells with impaired DDRs/genome damage continue dividing. Here, we show that continued division and normal organ development occurs in polyploid, DDR-impaired Drosophila papillar cells. As papillar cells become polyploid, they naturally accumulate broken acentric chromosomes but do not apoptose/arrest the cell cycle. To survive mitosis with acentric chromosomes, papillar cells require Fanconi anemia proteins FANCD2 and FANCI, as well as Blm helicase, but not canonical DDR signaling. FANCD2 acts independently of previous S phases to promote alignment and segregation of acentric DNA produced by double-strand breaks, thus avoiding micronuclei and organ malformation. Because polyploidy and impaired DDRs can promote cancer, our findings provide insight into disease-relevant DNA-damage tolerance mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.