ArticlePLoS genetics2011
Chk2 and p53 are haploinsufficient with dependent and independent functions to eliminate cells after telomere loss.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Selfish chromosomes exploit a germline checkpoint to eliminate competing gametes.Nature communications · 2026Article
- Genomic Perspective on Heterogeneity of Organs and Body Aging.Aging cell · 2026Review
- Nuclear reassembly defects after mitosis trigger apoptotic and p53-dependent safeguard mechanisms in Drosophila.PLoS biology · 2024Article
- Article
- Cullin-5 deficiency orchestrates the tumor microenvironment to promote mammary tumor development through CREB1-CCL2 signaling.Science advances · 2023Article
- Genetic alterations and their therapeutic implications in epithelial ovarian cancer.BMC cancer · 2021Article
- Identification and Characterization of Breakpoints and Mutations onG3 (Bethesda, Md.) · 2020Article
- Cells with loss-of-heterozygosity after exposure to ionizing radiation in Drosophila are culled by p53-dependent and p53-independent mechanisms.PLoS genetics · 2020Article
- Site-Specific Recombination with Inverted Target Sites: A Cautionary Tale of Dicentric and Acentric Chromosomes.Genetics · 2020Article
- Article
- P53 and Apoptosis in the Drosophila Model.Advances in experimental medicine and biology · 2019Review
- Overexpression of theHereditas · 2018Article
- Article
- Corp Regulates P53 in Drosophila melanogaster via a Negative Feedback Loop.PLoS genetics · 2015Article
- Chk2 and p53 regulate the transmission of healed chromosomes in the Drosophila male germline.PLoS genetics · 2014Article
- Multiple pathways suppress telomere addition to DNA breaks in the Drosophila germline.Genetics · 2012Article
- The generation of chromosomal deletions to provide extensive coverage and subdivision of the Drosophila melanogaster genome.Genome biology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms that cells use to monitor telomere integrity, and the array of responses that may be induced, are not fully defined. To date there have been no studies in animals describing the ability of cells to survive and contribute to adult organs following telomere loss. We developed assays to monitor the ability of somatic cells to proliferate and differentiate after telomere loss. Here we show that p53 and Chk2 limit the growth and differentiation of cells that lose a telomere. Furthermore, our results show that two copies of the genes encoding p53 and Chk2 are required for the cell to mount a rapid wildtype response to a missing telomere. Finally, our results show that, while Chk2 functions by activating the p53-dependent apoptotic cascade, Chk2 also functions independently of p53 to limit survival. In spite of these mechanisms to eliminate cells that have lost a telomere, we find that such cells can make a substantial contribution to differentiated adult tissues.
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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.