Fig. 5: Depletion of E2F1 induces DSBs and ssDNA gaps. | Experimental & Molecular Medicine

Fig. 5: Depletion of E2F1 induces DSBs and ssDNA gaps.

From: E2F1 facilitates DNA break repair by localizing to break sites and enhancing the expression of homologous recombination factors

Fig. 5

a Representative microscopic images of cells showing γH2AX foci in response to E2F1 knockdown. The nuclear perimeter was stained with DAPI (4′,6-diamidino-2-phenylindole). b Quantitative analysis of foci formed in response to E2F1 knockdown. The scatter plots illustrate the number of γH2AX foci per individual cell (mean ± SD), and a minimum of 150 nuclei were counted for each experiment. The number of foci per nucleus was analyzed using Prism5 software. ***P < 0.001 (Student’s t-test) indicates significance compared with siControl-treated cells. c Electron microscopic images showing replication forks isolated from Xenopus laevis (modified from Kolinjivadi et al. (2017)51). Following BRCA2 or RAD51 depletion, ~500 nucleotide-long ssDNA gaps are observed, but these gaps are not observed in control cells. d The proposed model by which E2F1-mediated HR factors maintain genomic integrity. When E2F1 activates HR factors by binding at their promoters, HR responds efficiently to induce DNA replication and DNA repair. E2F1 effectively localizes to DNA break sites, where it interacts with regulatory proteins involved in the HR pathway. However, E2F1 deficiency can cause replication fork collapse or the accumulation of DSBs or ssDNA gaps at S/G2 transition, inducing cell cycle arrest in G2/M phase or cell death

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