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Published on: June 6, 2017
Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation
Bing Pan1,2,3, Fanghua Li1,4, Emil Mladenov1,2
1Institute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Iscience
|July 12, 2026
Summary
Cell cycle phase dictates DNA repair pathway choice. Polo-like kinase 1 (PLK1) controls DNA end resection in S-phase, while PLK1 and PLK3 redundantly regulate it in G2-phase, impacting DNA double-strand break repair.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- DNA double-strand breaks (DSBs) are critical DNA lesions.
- Homologous recombination (HR) and non-homologous end joining (NHEJ) are primary DSB repair pathways.
- Alternative end joining (alt-EJ) and single-strand annealing (SSA) serve as backup repair mechanisms.
Purpose of the Study:
- To investigate the cell-cycle-dependent regulation of DNA double-strand break repair pathway choice.
- To identify the roles of Polo-like kinases (PLKs) in controlling DNA end resection during different cell cycle phases.
Main Methods:
- Irradiation of human cells to induce DSBs.
- Pharmacological inhibition of PLK1.
- Protein depletion techniques to assess PLK3 function.
- Analysis of DNA end resection dynamics across the cell cycle.
Main Results:
- PLK1 alone regulates DNA end resection in S-phase following irradiation.
- PLK1 and PLK3 act redundantly to control resection in G2-phase irradiated cells.
- This regulation is independent of SCFSKP2-APC/CCDH1-mediated CtIP modulation.
Conclusions:
- PLK1 and PLK3 are key cell-cycle-dependent regulators of DSB repair pathway selection.
- Differential PLK activity couples cell-cycle progression to DNA repair decisions.
- Findings advance the understanding of DNA repair mechanisms and cell cycle checkpoints.
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