Journal Article

DKFZ-2026-01712

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.

Pan, B. ; Li, F.DKFZ* ; Mladenov, E. ; Stuschke, M.DKFZ* ; Timmermann, B.DKFZ* ; Iliakis, G.

2026
Elsevier St. Louis

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 SCFSKP2-APC/CCDH1-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.

Keyword(s): Cell biology ; DSB repairs ; Molecular interaction ; Molecular network

Note: #DKTKZFB26#

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Contributing Institute(s):

1. DKTK Koordinierungsstelle Essen/Düsseldorf (ED01)

Research Program(s):

1. 899 - ohne Topic (POF4-899) (POF4-899)

Appears in the scientific report 2026

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Database coverage:
; ; Article Processing Charges ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DOAJ Seal ; Essential Science Indicators ; Fees ; IF >= 5 ; JCR ; PubMed Central ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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