Figure 2.

The SOG1-independent DDR signalling appears to favour the onset of DNA damage repair mechanisms. RBR, together with E2FA are key regulators of both cell cycle and DDR genes in the absence of DNA lesions [62]. Upon DNA damage, the SOG1 transcription factor overtakes the transcriptional regulation response to fine-tune DDR signalling. Thus, among hundreds of targets, the WEE1 kinase, other ANAC transcription factors or CKI proteins, such as SMR4, SMR5, SMR7, and KRP6, are activated. By inhibiting the CDK/CYC complex, other regulators, such as the Rep-MYBs, are not further phosphorylated, and these TFs accumulate in the cell, hence, contributing to block the cell cycle progression. Then, to avoid the transmission of damaged DNA, the cell will either switch towards endoreduplication or proceed to DNA lesion repair. In this option, the RBR-E2F pathway can be activated to setup DNA repair mainly by homologous recombination, this signalling pathway could be activated either via the activity of the CDKB1;1/CYCB1;1 complex, or via a SOG1-independent activation from upstream components not yet identified. Finally, if none of these alternatives is reached, then cell death will occur. A question mark (?) indicates that further experimental data are needed for confirmation of the indicated connections.