ArticleCell cycle (Georgetown, Tex.)2010
Revised genetic requirements for the decatenation G2 checkpoint: the role of ATM.
Article in Cell cycle (Georgetown, Tex.), 2010. 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, 27 citations in OpenAlex.
- Targeting the ERα DBD-LBD Interface with Mitoxantrone Disrupts Receptor Function through Proteasomal Degradation.Molecular cancer therapeutics · 2026Article
- AAV vector transduction restriction and attenuated toxicity in hESCs via a rationally designed inverted terminal repeat.Nucleic acids research · 2025Article
- Cell cycle responses to Topoisomerase II inhibition: Molecular mechanisms and clinical implications.The Journal of cell biology · 2023Review
- Dysregulated G2 phase checkpoint recovery pathway reduces DNA repair efficiency and increases chromosomal instability in a wide range of tumours.Oncogenesis · 2021Article
- Review
- Review
- MCPH1 is essential for cellular adaptation to the GFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- A genome-wide RNAi screen identifies the SMC5/6 complex as a non-redundant regulator of a Topo2a-dependent G2 arrest.Nucleic acids research · 2019Article
- Patterns of cell cycle checkpoint deregulation associated with intrinsic molecular subtypes of human breast cancer cells.NPJ breast cancer · 2017Article
- Effective intra-S checkpoint responses to UVC in primary human melanocytes and melanoma cell lines.Pigment cell & melanoma research · 2016Article
- Catalytic inhibitors of DNA topoisomerase II suppress the androgen receptor signaling and prostate cancer progression.Oncotarget · 2015Article
- Titanium dioxide nanoparticles activate the ATM-Chk2 DNA damage response in human dermal fibroblasts.Nanotoxicology · 2013Article
- Ataxia telangiectasia mutated-dependent regulation of topoisomerase II alpha expression and sensitivity to topoisomerase II inhibitor.Cancer science · 2013Article
- Direct monitoring of the strand passage reaction of DNA topoisomerase II triggers checkpoint activation.PLoS genetics · 2013Article
- Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.Oncotarget · 2012Review
- Mitosis in vertebrates: the G2/M and M/A transitions and their associated checkpoints.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2011Review
- Topoisomerase IIalpha maintains genomic stability through decatenation G(2) checkpoint signaling.Oncogene · 2010Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The decatenation G2 checkpoint is proposed to delay cellular progression from G2 into mitosis when intertwined daughter chromatids are insufficiently decatenated. Previous studies indicated that the ATM- and Rad3-related (ATR) checkpoint kinase, but not the ataxia telangiectasia-mutated (ATM) kinase, was required for decatenation G2 checkpoint function. Here, we show that the method used to quantify decatenation G2 checkpoint function can influence the identification of genetic requirements for the checkpoint. Normal human diploid fibroblast (NHDF) lines responded to the topoisomerase II (topo II) catalytic inhibitor ICRF-193 with a stringent G2 arrest and a reduction in the mitotic index. While siRNA-mediated depletion of ATR and CHEK1 increased the mitotic index in ICRF-193 treated NHDF lines, depletion of these proteins did not affect the mitotic entry rate, indicating that the decatenation G2 checkpoint was functional. These results suggest that ATR and CHEK1 are not required for the decatenation G2 checkpoint, but may influence mitotic exit after inhibition of topo II. A re-evaluation of ataxia telangiectasia (AT) cell lines using the mitotic entry assay indicated that ATM was required for the decatenation G2 checkpoint. Three NHDF cell lines responded to ICRF-193 with a mean 98% inhibition of the mitotic entry rate. Examination of the mitotic entry rates in AT fibroblasts upon treatment with ICRF-193 revealed a significantly attenuated decatenation G2 checkpoint response, with a mean 59% inhibition of the mitotic entry rate. In addition, a normal lymphoblastoid line exhibited a 95% inhibition of the mitotic entry rate after incubation with ICRF-193, whereas two AT lymphoblastoid lines displayed only 36% and 20% inhibition of the mitotic entry rate. Stable depletion of ATM in normal human fibroblasts with short hairpin RNA also attenuated decatenation G2 checkpoint function by an average of 40%. Western immunoblot analysis demonstrated that treatment with ICRF-193 induced ATM autophosphorylation and ATM-dependent phosphorylation of Ser15-p53 and Thr68 in Chk2, but no appreciable phosphorylation of Ser139-H2AX or Ser345-Chk1. The results suggest that inhibition of topo II induces ATM to phosphorylate selected targets that contribute to a G2 arrest independently of DNA damage.
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