Fig. 4.

Notch-induced autophagy and translational noise as destabilizers of cellular memory. a The schematic diagram demonstrates molecular interactions that regulate transitioning between pro-anabolic and pro-catabolic states in a cell. b Subsequent to activation of Notch signalling, the PTEN^high and PTEN^low temporal windows (corresponding to the Notch^on state of Fig. 2c) accommodate pro-catabolic (high autophagy) and pro-anabolic (high protein synthesis) phases. c Notch signals facilitate G0/G1 transition by upregulating Myc and cyclin D1. On the other hand, Notch signals inhibit G1/S transition. In consequence, cycling cells dwell longer in noisy G1 characterized by amplified protein synthesis