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The cell cycle-dependent engagement of DNA-end resection at DSBs is regulated by phosphorylation of CTIP by CDKs, the central regulators of cell cycle transitions. Cell cycle transitions are also intimately regulated by protein degradation via two E3 ubiquitin ligases: SCF SKP2  and APC/C CDH1  complex. Although APC/C CDH1  regulates CTIP in G 1 – and G 2 -phase, contributions by SCF SKP2  have not been reported. We demonstrate that SCF SKP2  is a strong positive regulator of resection. Knockdown of SKP2, fully suppresses resection in several cell lines. Notably, this suppression is G 2 -phase specific and is not observed in S-phase or G 1 –phase cells. Knockdown of SKP2 inactivates SCF SKP2  causing APC/C CDH1  activation, which degrades CTIP. The stabilizing function of SCF SKP2  on CTIP promotes resection and supports gene conversion (GC), alternative end joining (alt-EJ) and cell survival. We propose that CDKs and SCF SKP2 -APC/C CDH1  cooperate to regulate resection and repair pathway choice at DSBs in G 2 -phase.

SCFSKP2 regulates APC/CCDH1-mediated degradation of CTIP to adjust DNA-end resection in G2-phase