Figure 1

Inter-relationships between reversible polyploidy, senescence and stemness. This diagram highlights the inter-relationships and shared molecular pathways between the three processes of polyploidy, senescence and stemness. DNA damage potentiates this process leading to arrest at the G2M damage checkpoint from which cells that by-pass mitotic catastrophe go on to enter the polyploid cycle, eliciting transient stemness to overcome senescence. TP53 serves as a strong negative regulator of the process, favouring arrest at G1, apoptosis induction and inhibiting entry into polyploidy.