ArticleGenes & development2004
Drosophila atm/telomere fusion is required for telomeric localization of HP1 and telomere position effect.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 105 citations in OpenAlex.
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- Telomere Checkpoint in Development and Aging.International journal of molecular sciences · 2023Review
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- Kinetochore-independent mechanisms of sister chromosome separation.PLoS genetics · 2021Article
- Overexpression of theHereditas · 2018Article
- dAdd1 and dXNP prevent genome instability by maintaining HP1a localization at Drosophila telomeres.Chromosoma · 2017Article
- AnOpen biology · 2017Article
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- Recurrent Innovation at Genes Required for Telomere Integrity in Drosophila.Molecular biology and evolution · 2017Article
- Whole-Genome Sequencing and iPLEX MassARRAY Genotyping Map an EMS-Induced Mutation Affecting Cell Competition in Drosophila melanogaster.G3 (Bethesda, Md.) · 2016Article
- Drosophila Wnt and STAT Define Apoptosis-Resistant Epithelial Cells for Tissue Regeneration after Irradiation.PLoS biology · 2016Article
- Corp Regulates P53 in Drosophila melanogaster via a Negative Feedback Loop.PLoS genetics · 2015Article
- The Analysis of Pendolino (peo) Mutants Reveals Differences in the Fusigenic Potential among Drosophila Telomeres.PLoS genetics · 2015Article
- Article
- If the cap fits, wear it: an overview of telomeric structures over evolution.Cellular and molecular life sciences : CMLS · 2014Review
- Dying cells protect survivors from radiation-induced cell death in Drosophila.PLoS genetics · 2014Article
- Article
- The tumor suppressor Caliban regulates DNA damage-induced apoptosis through p53-dependent and -independent activity.Oncogene · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Terminal deletions of Drosophila chromosomes can be stably protected from end-to-end fusion despite the absence of all telomere-associated sequences. The sequence-independent protection of these telomeres suggests that recognition of chromosome ends might contribute to the epigenetic protection of telomeres. In mammals, Ataxia Telangiectasia Mutated (ATM) is activated by DNA damage and acts through an unknown, telomerase-independent mechanism to regulate telomere length and protection. We demonstrate that the Drosophila homolog of ATM is encoded by the telomere fusion (tefu) gene. In the absence of ATM, telomere fusions occur even though telomere-specific Het-A sequences are still present. High levels of spontaneous apoptosis are observed in ATM-deficient tissues, indicating that telomere dysfunction induces apoptosis in Drosophila. Suppression of this apoptosis by p53 mutations suggests that loss of ATM activates apoptosis through a DNA damage-response mechanism. Loss of ATM reduces the levels of heterochromatin protein 1 (HP1) at telomeres and suppresses telomere position effect. We propose that recognition of chromosome ends by ATM prevents telomere fusion and apoptosis by recruiting chromatin-modifying complexes to telomeres.
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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.