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. 2012 Jul 27;31(16):3380–3381. doi: 10.1038/emboj.2012.199

Figure 1.

Figure 1

Telomere damage signalling at the G2/M transition. Telomeres uncapped through POT1 or TRF2 depletion activate ATR or ATM signalling, respectively, leading to CHK1- or CHK2-dependent CDC25A or CDC25C phosphorylation. This targets CDC25 phosphatases for ubiquitin-proteasome-mediated degradation either directly (CDC25A) or following export into the cytoplasm (CDC25C). As a consequence, inhibitory CDK1 Tyr15 phosphorylation persists, blocking progression into mitosis. IR-induced DSBs activate both ATM and ATR, but selectively affect CDC25A stability.