Figure 1. Parallelisms between quiescence deepening and L1 ageing. (A) Upon removal of growth factors, REF (Rat Embryonic Fibroblast) enter cell quiescence, a reversible, non-proliferative state. Cells progressively undergo quiescence deepening as they accumulate ROS and protein aggregates. After prolonged quiescence, cells require stronger stimulation and take longer to exit quiescence and return to proliferation. Eventually cells reach senescence, an irreversible state of cell arrest. (B) L1 arrested C. elegans larvae show a similar process to quiescence deepening. Prolonged arrest entails a process named L1 aging, that also involves accumulation of ROS and protein aggregates. We have shown that prolonged quiescence leads to a delay in the initiation of postembryonic cell divisions. Before dying as arrested L1, larvae lose the capacity to recover from L1 arrest, a process that could be compared to cell senescence. (C) Insulin signalling modulated the process of L1 aging. Activation of the transcription factor DAF-16, as that sound in daf-2 mutants, leads to a slower rate of L1 aging. As a consequence, after the same time in L1 arrest, daf-2 mutants accumulate less markers of aging. This allows a faster recovery once larvae encounter food. daf-16 mutants, show faster L1 ageing and the initiation of postembryonic divisions upon feeding is delayed compared to the wild type.