Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.

Authors

Bing Pan, Fanghua Li, Emil Mladenov, Martin Stuschke, Beate Timmermann, George Iliakis

Published in

iScience. Volume 29. Issue 7. Pages 116450. Jul 17, 2026. Epub Jul 01, 2026.

Abstract

DNA double-strand breaks (DSBs) are highly cytotoxic lesions repaired primarily by homologous recombination (HR) and non-homologous end joining (NHEJ), with alternative end joining (alt-EJ) and single-strand annealing (SSA) functioning as backup. Repair pathway choice is governed by DNA end resection, suppressing NHEJ and committing repair to homology-based processes. Using pharmacological inhibition and protein depletion approaches in irradiated human cells, we show that PLK1 alone controls resection in S-phase-irradiated cells, while PLK1 and PLK3 act redundantly in G₂-phase-irradiated cells. This cell-cycle-dependent regulation operates through a mechanism distinct from SCF^SKP2-APC/C^CDH1-mediated CtIP level modulation. These findings establish PLK1 and PLK3 as cell-cycle-dependent regulators of DSB repair pathway choice, advancing our understanding of how cell-cycle progression is coupled to repair decisions through differential PLK activity.

PMID:
42436985
Bibliographic data and abstract were imported from PubMed on 12 Jul 2026.

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