Cited by 207Planarian Biology and ElectrostimulationDevelopmental Biology and Gene RegulationWound Healing and Treatments

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Lack of p21 expression links cell cycle control and appendage regeneration in mice

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Bedelbaeva, Khamilia, Snyder, Andrew, Gourevitch, Dmitri, Clark, Lise, Zhang, Xiang-Ming, Leferovich, John, Cheverud, James M., Lieberman, Paul, Heber-Katz, Ellen·2010·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1000830107PMC PMC2851923

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Abstract

Animals capable of regenerating multiple tissue types, organs, and appendages after injury are common yet sporadic and include some sponge, hydra, planarian, and salamander (i.e., newt and axolotl) species, but notably such regenerative capacity is rare in mammals. The adult MRL mouse strain is a rare exception to the rule that mammals do not regenerate appendage tissue. Certain commonalities, such as blastema formation and basement membrane breakdown at the wound site, suggest that MRL mice may share other features with classical regenerators. As reported here, MRL fibroblast-like cells have a distinct cell-cycle (G2/M accumulation) phenotype and a heightened basal and wound site DNA damage/repair response that is also common to classical regenerators and mammalian embryonic stem cells. Additionally, a neutral and alkaline comet assay displayed a persistent level of intrinsic DNA damage in cells derived from the MRL mouse. Similar to mouse ES cells, the p53-target p21 was not expressed in MRL ear fibroblasts. Because the p53/p21 axis plays a central role in the DNA damage response and cell cycle control, we directly tested the hypothesis that p21 down-regulation could functionally induce a regenerative response in an appendage of an otherwise nonregenerating mouse strain. Using the ear hole closure phenotype, a genetically mapped and reliable quantitative indicator of regeneration in the MRL mouse, we show that the unrelated Cdkn1a tmi/Tyj /J p21 −/− mouse (unlike the B6129SF2/J WT control) closes ear holes similar to MRL mice, providing a firm link between cell cycle checkpoint control and tissue regeneration.

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Authors: Bedelbaeva, K., Snyder, A., Gourevitch, D., Clark, L., Zhang, X.-M., Leferovich, J., Cheverud, J. M., Lieberman, P., & Heber-Katz, E.
Affiliations: The Wistar Institute (US)
Cellular and Molecular Oncogenesis and Gene Expression, The Wistar Institute, Philadelphia, PA 19104; and
Washington University in St. Louis (US)
ORCID: Snyder, Andrew
Cheverud, James M.
Lieberman, Paul
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2010-03-15
Volume: 107
Issue: 13
Pages: 5845-5850
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.1000830107
PMC: PMC2851923
OpenAlex: W2120729899
Cited by: 207
References: 61
Citations by year: 2026: 3 · 2025: 9 · 2024: 5 · 2023: 6 · 2022: 11 · 2021: 8 · 2020: 11 · 2019: 11 · 2018: 11 · 2017: 16 · 2016: 14 · 2015: 27 · 2014: 13 · 2013: 22 · 2012: 17
FWCI: 7.95
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: F. M. Kirby Foundation
James N. Kirby Foundation
National Institutes of Health (CA 10815)
National Cancer Institute ((P30 CA10815, CA-10815, P30CA010815)
National Institute of General Medical Sciences (R01GM073226, GM073226)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Planarian Biology and Electrostimulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Health Sciences › Medicine › Surgery › Wound Healing and Treatments
Keywords: p21, p53, appendage regeneration, cell cycle regulation, DNA damage response, fibroblasts, blastema formation, wound healing, cell cycle checkpoints, DNA repair
MeSH terms: Animals, Cell Cycle, Cell Division, DNA Damage, DNA Repair, Extremities, Female, Mice, Inbred C57BL, Regeneration, Tumor Suppressor Protein p53, G2 Phase, Apoptosis, Mice, Knockout, Mice, Congenic, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p21, Rad51 Recombinase, Mice, Protein Stability, In Vitro Techniques

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Lack of p21 expression links cell cycle control and appendage regeneration in mice

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