Figures & data
Figure 1. Model of the coupling between signaling, post-transcriptional regulation, and cell fate control by the ERK-LIN28 axis. Left: In the absence of fibroblast growth factor (FGF), ERK is inactive, LIN28 is not phosphorylated and thus expressed at a lower level, whereby it can bind and inhibit the processing of let-7 precursors (pre-let-7) and engage with some of its direct mRNA targets to modulate their translation. Right: Upon FGF stimulation, ERK is activated and phosphorylates LIN28, which increases LIN28s protein levels, allowing it to engage with more mRNA targets and enhancing its effect on translation. As indicated on the bottom, this mechanism facilitates the transition from naïve to primed pluripotency.
