p130/p107/p105Rb-dependent transcriptional repression during DNA-damage-induced cell-cycle exit at G2

Jackson, Mark W.; Agarwal, Mukesh K.; Yang, Jinbo; Bruss, Patrick; Uchiumi, Takeshi; Agarwal, Munna L.; Stark, George R.; Taylor,, William R.

doi:10.1242/jcs.02307

Cited by 92Cancer-related Molecular PathwaysDNA Repair MechanismsMicrotubule and mitosis dynamics

p130/p107/p105Rb-dependent transcriptional repression during DNA-damage-induced cell-cycle exit at G2

Jackson, Mark W., Agarwal, Mukesh K., Yang, Jinbo, Bruss, Patrick, Uchiumi, Takeshi, Agarwal, Munna L., Stark, George R., Taylor,, William R.·2005·Journal of Cell Science

DOI 10.1242/jcs.02307

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Abstract

The progression of normal cells from G2 into mitosis is stably blocked when their DNA is damaged. Tumor cells lacking p53 arrest only transiently in G2, but eventually enter mitosis. We show that an important component of the stable G2 arrest in normal cells is the transcriptional repression of more than 20 genes encoding proteins needed to enter into and progress through mitosis. Studies from a number of labs including our own have shown that, by inducing p53 and p21/WAF1, DNA damage can trigger RB-family-dependent transcriptional repression. Our studies reported here show that p130 and p107 play a key role in transcriptional repression of genes required for G2 and M in response to DNA damage. For plk1, repression is partially abrogated by loss of p130 and p107, and is completely abrogated by loss of all three RB-family proteins. Mouse cells lacking RB-family proteins do not accumulate with a 4N content of DNA when exposed to adriamycin, suggesting that all three RB-family proteins contribute to G2 arrest in response to DNA damage. Stable arrest in the presence of functional p53-to-RB signaling is probably due to the ability of cells to exit the cell cycle from G2, a conclusion supported by our observation that KI67, a marker of cell-cycle entry, is downregulated in both G1 and G2 in a p53-dependent manner.

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Downregulation of mitotic regulators after G2 arrest is due both to pRb-mediated suppression and to protein degradation by APC/C-Cdh1.
“Originally, downregulation of mitotic regulators following G2 arrest was attributed to pRb-mediated suppression of their expression 64 (Fig. 2).However, subsequent work in several laboratories provided evidence that this is also due to protein degradation triggered by anaphase-promoting complex/cyclosome (APC/C) and its co-activator Cdh1 [74][75][76] (Fig. 2).”
From Senescence from G2 arrest, revisited (2015) · cites this paper as [64]

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RB, p130 and p107 differentially repress G1/S and G2/M genes after p53 activation
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Cell cycle regulatory genes are principal targets of p53-dependent, RB-mediated transcriptional repression following DNA damage
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Self-citation

Authors: Jackson, M. W., Agarwal, M. K., Yang, J., Bruss, P., Uchiumi, T., Agarwal, M. L., Stark, G. R., & Taylor
Affiliations: Cleveland Clinic (US)
Kyushu University (JP)
Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
ORCID: Jackson, Mark W.
Uchiumi, Takeshi
Stark, George R.
Venue: Journal of Cell Science
Publisher: The Company of Biologists
Published: 2005-05-01
Volume: 118
Issue: 9
Pages: 1821-1832
ISSN: 0021-9533 (ISSN-L)
1477-9137
DOI: 10.1242/jcs.02307
OpenAlex: W2005261085
Cited by: 92
References: 69
Citations by year: 2025: 2 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 4 · 2019: 4 · 2018: 1 · 2017: 3 · 2015: 4 · 2014: 3 · 2013: 7 · 2012: 7
FWCI: 3.75
Type: journal article
Language: en
Open access: closed
Locations: Journal of Cell Science (publishedVersion)
PubMed (publishedVersion)
HighWire Press Open Archive (submittedVersion)
Funders: National Institute of General Medical Sciences (GM49345, R01GM049345)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
Keywords: p130, p107, Rb family proteins, transcriptional repression, DNA damage, G2 cell cycle arrest, cell cycle exit, p53, p21, PLK1, mitosis entry, doxorubicin, Ki-67
MeSH terms: Animals, Antibiotics, Antineoplastic, Cell Cycle, Cell Separation, DNA, DNA Damage, Doxorubicin, Flow Cytometry, Humans, Mitosis, Models, Biological, Nuclear Proteins, Protein Binding, Proteins, Time Factors, Transcription, Genetic, Blotting, Northern, Blotting, Western, Signal Transduction, Down-Regulation, Tumor Suppressor Protein p53, Retinoblastoma Protein, G2 Phase, Cell Cycle Proteins, Ki-67 Antigen, Cell Proliferation, Retinoblastoma-Like Protein p130, Retinoblastoma-Like Protein p107, Cyclin-Dependent Kinase Inhibitor p21, Mice

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p130/p107/p105Rb-dependent transcriptional repression during DNA-damage-induced cell-cycle exit at G2

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