The Tumor Suppressor PML Specifically Accumulates at RPA/Rad51-Containing DNA Damage Repair Foci but Is Nonessential for DNA Damage-Induced Fibroblast Senescence
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The PML tumor suppressor has been functionally implicated in DNA damage response and cellular senescence. Direct evidence for such a role based on PML knockdown or knockout approaches is still lacking. We have therefore analyzed the irradiation-induced DNA damage response and cellular senescence in human and mouse fibroblasts lacking PML. Our data show that PML nuclear bodies (NBs) nonrandomly associate with persistent DNA damage foci in unperturbed human skin and in high-dose-irradiated cell culture systems. PML bodies do not associate with transient γH2AX foci after low-dose gamma irradiation. Superresolution microscopy reveals that all PML bodies within a nucleus are engaged at Rad51- and RPA-containing repair foci during ongoing DNA repair. The lack of PML (i) does not majorly affect the DNA damage response, (ii) does not alter the efficiency of senescence induction after DNA damage, and (iii) does not affect the proliferative potential of primary mouse embryonic fibroblasts during serial passaging. Thus, while PML NBs specifically accumulate at Rad51/RPA-containing lesions and senescence-derived persistent DNA damage foci, they are not essential for DNA damage-induced and replicative senescence of human and murine fibroblasts.
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RAD51 encodes a DNA repair enzyme that associates with gH2AX foci.
“RAD51 (FC = 1.2, p = 0.05) encodes a DNA repair enzyme which associate with gH2AX foci [103].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [103]
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Legartová, S., Sehnalová, P., Malyšková, B., Küntziger, T. M., Collas, P., Cmarko, D., Raška, I., Sorokin, D. V., Kozubek, S., & Bártová, E. (2016) · Journal of Cellular Biochemistry · doi:10.1002/jcb.25551 · Cited by 7 · see citing works
Phospho-SIM and exon8b of PML protein regulate formation of doxorubicin-induced rDNA-PML compartment
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PARP5B is required for nonhomologous end joining during tumorigenesis in vivo
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Effects of ebselen and N-acetyl cysteine on replicative aging of primary human fibroblast strains
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Biomarkers of Replicative Senescence Revisited
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- Authors
- Münch, S., Weidtkamp-Peters, S., Klement, K., Grigaravicius, P., Monajembashi, S., Salomoni, P., Pandolfi, P. P., Weißhart, K., & Hemmerich, P.
- Affiliations
- Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) (DE)
- Leibniz Institute for Age Research, Jena, Germany
- University College London (GB)
- Beth Israel Deaconess Medical Center (US)
- Carl Zeiss Microscopy GmbH, BioSciences Division, Jena, Germany
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2014-05-01
- Volume
- 34
- Issue
- 10
- Pages
- 1733-1746
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC4019039
- OpenAlex
- W2124037118
- Cited by
- 32
- References
- 74
- Citations by year
- 2024: 3 · 2023: 5 · 2022: 1 · 2021: 2 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 7 · 2015: 5 · 2014: 3
- FWCI
- 2.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Brain Tumour Charity
- Bundesministerium für Bildung und Forschung
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- PML nuclear bodies, DNA damage response, DNA repair foci, RAD51, RPA, replicative senescence, fibroblast senescence, gamma irradiation, γH2AX foci, super-resolution microscopy
- MeSH terms
- Promyelocytic Leukemia Protein, Animals, Cell Line, Cell Nucleus, DNA Damage, DNA Repair, Fibroblasts, Histones, Humans, Nuclear Proteins, Transcription Factors, Cellular Senescence, Protein Transport, Tumor Suppressor Proteins, Cell Proliferation, Rad51 Recombinase, Mice, Replication Protein A
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