ArticleGenetics2008
Telomere loss provokes multiple pathways to apoptosis and produces genomic instability in Drosophila melanogaster.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
The trial behind it
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
50 citing papers in PubMed, 73 citations in OpenAlex.
- Dual contributions of Xrp1 to genome integrity through the DNA damage response and cell competition.PLoS genetics · 2026Article
- Determinants of dicentric chromosome breakage inbioRxiv : the preprint server for biology · 2026Article
- Broken chromosomes heading into mitosis: More than one way to patch a flat tire.The Journal of cell biology · 2024Review
- Ribosomal protein mutations and cell competition: autonomous and nonautonomous effects on a stress response.Genetics · 2023Article
- Article
- Connections between sister and non-sister telomeres of segregating chromatids maintain euploidy.Current biology : CB · 2023Article
- Review
- Reducing the aneuploid cell burden - cell competition and the ribosome connection.Disease models & mechanisms · 2022Review
- Article
- Regulation and coordination of the different DNA damage responses inFrontiers in cell and developmental biology · 2022Review
- Article
- Mechanisms driving acentric chromosome transmission.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020Review
- Site-Specific Recombination with Inverted Target Sites: A Cautionary Tale of Dicentric and Acentric Chromosomes.Genetics · 2020Article
- Outcompeting cancer.Nature reviews. Cancer · 2020Review
- IT'S 2 for the price of 1: Multifaceted ITS2 processing machines in RNA and DNA maintenance.DNA repair · 2019Review
- Article
- P53 and Apoptosis in the Drosophila Model.Advances in experimental medicine and biology · 2019Review
- Xrp1 is a transcription factor required for cell competition-driven elimination of loser cells.Scientific reports · 2018Article
- Article
- Micronuclei Formation Is Prevented by Aurora B-Mediated Exclusion of HP1a from Late-Segregating Chromatin inGenetics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Telomere loss was produced during development of Drosophila melanogaster by breakage of an induced dicentric chromosome. The most prominent outcome of this event is cell death through Chk2 and Chk1 controlled p53-dependent apoptotic pathways. A third p53-independent apoptotic pathway is additionally utilized when telomere loss is accompanied by the generation of significant aneuploidy. In spite of these three lines of defense against the proliferation of cells with damaged genomes a small fraction of cells that have lost a telomere escape apoptosis and divide repeatedly. Evasion of apoptosis is accompanied by the accumulation of karyotypic abnormalites that often typify cancer cells, including end-to-end chromosome fusions, anaphase bridges, aneuploidy, and polyploidy. There was clear evidence of bridge-breakage-fusion cycles, and surprisingly, chromosome segments without centromeres could persist and accumulate to high-copy number. Cells manifesting these signs of genomic instability were much more frequent when the apoptotic mechanisms were crippled. We conclude that loss of a single telomere is sufficient to generate at least two phenotypes of early cancer cells: genomic instability that involves multiple chromosomes and aneuploidy. This aneuploidy may facilitate the continued escape of such cells from the normal checkpoint 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.