ATM Is Required for Telomere Maintenance and Chromosome Stability during Drosophila Development
Current Biology, ISSN: 0960-9822, Vol: 14, Issue: 15, Page: 1341-1347
2004
- 90Citations
- 53Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations90
- Citation Indexes90
- 90
- CrossRef88
- Captures53
- Readers53
- 53
Article Description
ATM is a large, multifunctional protein kinase that regulates responses required for surviving DNA damage: including DNA repair, apoptosis, and cell cycle checkpoints [1]. Here, we show that Drosophila ATM function is essential for normal adult development. Extensive, inappropriate apoptosis occurs in proliferating atm mutant tissues, and in clonally derived atm mutant embryos, frequent mitotic defects were seen. At a cellular level, spontaneous telomere fusions and other chromosomal abnormalities are common in atm larval neuroblasts, suggesting a conserved and essential role for dATM in the maintenance of normal telomeres and chromosome stability. Evidence from other systems supports the idea that DNA double-strand break (DSB) repair functions of ATM kinases promote telomere maintenance by inhibition of illegitimate recombination or fusion events between the legitimate ends of chromosomes and spontaneous DSBs [2–4]. Drosophila will be an excellent model system for investigating how these ATM-dependent chromosome structural maintenance functions are deployed during development. Because neurons appear to be particularly sensitive to loss of ATM in both flies and humans, this system should be particularly useful for identifying cell-specific factors that influence sensitivity to loss of dATM and are relevant for understanding the human disease, ataxia-telangiectasia.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0960982204004695; http://dx.doi.org/10.1016/j.cub.2004.06.056; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=4143123447&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15296750; https://linkinghub.elsevier.com/retrieve/pii/S0960982204004695; https://dx.doi.org/10.1016/j.cub.2004.06.056
Elsevier BV
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