Optogenetic clustering of CNK1 reveals mechanistic insights in RAF and AKT signalling controlling cell fate decisions

Sci Rep.      online article

Using light-controllable CNK1, optoCNK1, we demonstrate that CNK1 acts as platform for different signaling complexes and allows switching between stimulation of ERK and AKT signaling dependent on the light intensity applied. Similar to the light intensity the dose of EGF induces a change in CNK1 complex composition and thereby allows RAF/ERK signaling or exertion of an AKT/RAF crosstalk which suppresses RAF/ERK signaling. Analyzing C2 skeletal muscle cells and MCF7 breast cancer cells we demonstrate that CNK1 expression and CNK1-mediated signaling decide on proliferation versus differentiation in a cell type- and cell stage-dependent manner.