Next Article in Journal
An Insight into the Mechanism of Holamine- and Funtumine-Induced Cell Death in Cancer Cells
Next Article in Special Issue
Stacking Effects on Anthraquinone/DNA Charge-Transfer Electronically Excited States
Previous Article in Journal
Bioactive Agent Discovery from the Natural Compounds for the Treatment of Type 2 Diabetes Rat Model
Previous Article in Special Issue
Tracing the Photoaddition of Pharmaceutical Psoralens to DNA

DNA Damaged Induced Cell Death in Oocytes

Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University, 60438 Frankfurt, Germany
Department for Gynecological Endocrinology and Reproductive Medicine, University Hospital of Bonn, Venusberg-Campus 1, 53217 Bonn, Germany
Institute for Genome Stability in Aging and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center, and Center for Molecular Medicine, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany
Author to whom correspondence should be addressed.
Present address: The Francis Crick Institute, London NW1 1AT, UK.
Academic Editors: Daniel Roca-Sanjuán, Virginie L. Lhiaubet-Vallet and Iñaki Tuñón
Molecules 2020, 25(23), 5714;
Received: 25 August 2020 / Revised: 25 November 2020 / Accepted: 30 November 2020 / Published: 3 December 2020
(This article belongs to the Special Issue DNA Damage and Repair)
The production of haploid gametes through meiosis is central to the principle of sexual reproduction. The genetic diversity is further enhanced by exchange of genetic material between homologous chromosomes by the crossover mechanism. This mechanism not only requires correct pairing of homologous chromosomes but also efficient repair of the induced DNA double-strand breaks. Oocytes have evolved a unique quality control system that eliminates cells if chromosomes do not correctly align or if DNA repair is not possible. Central to this monitoring system that is conserved from nematodes and fruit fly to humans is the p53 protein family, and in vertebrates in particular p63. In mammals, oocytes are stored for a long time in the prophase of meiosis I which, in humans, can last more than 50 years. During the entire time of this arrest phase, the DNA damage checkpoint remains active. The treatment of female cancer patients with DNA damaging irradiation or chemotherapeutics activates this checkpoint and results in elimination of the oocyte pool causing premature menopause and infertility. Here, we review the molecular mechanisms of this quality control system and discuss potential therapeutic intervention for the preservation of the oocyte pool during chemotherapy. View Full-Text
Keywords: p63; p73; p53 family; CEP-1; tetramerization; transcriptional activity; oocyte death; development; quality control p63; p73; p53 family; CEP-1; tetramerization; transcriptional activity; oocyte death; development; quality control
Show Figures

Figure 1

MDPI and ACS Style

Gebel, J.; Tuppi, M.; Sänger, N.; Schumacher, B.; Dötsch, V. DNA Damaged Induced Cell Death in Oocytes. Molecules 2020, 25, 5714.

AMA Style

Gebel J, Tuppi M, Sänger N, Schumacher B, Dötsch V. DNA Damaged Induced Cell Death in Oocytes. Molecules. 2020; 25(23):5714.

Chicago/Turabian Style

Gebel, Jakob, Marcel Tuppi, Nicole Sänger, Björn Schumacher, and Volker Dötsch. 2020. "DNA Damaged Induced Cell Death in Oocytes" Molecules 25, no. 23: 5714.

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop