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Netrin-1 promotes naive pluripotency through Neo1 and Unc5b co-regulation of Wnt and MAPK signallingHuyghe, Aurélia; Furlan, Giacomo; Ozmadenci, Duygu; Galonska, Christina; Charlton, Jocelyn; Gaume, Xavier; Combémorel, Noémie; Riemenschneider, Christina; Allègre, Nicolas; Zhang, Jenny; Wajda, Pauline; Rama, Nicolas; Vieugué, Pauline; Durand, Isabelle; Brevet, Marie; Gadot, Nicolas; Imhof, Thomas; Merrill, Bradley J; Koch, Manuel; Mehlen, Patrick; Chazaud, Claire; Meissner, Alexander; Lavial, Fabrice
Nature cell biology, 04/2020, Letnik: 22, Številka: 4Journal Article
In mouse embryonic stem cells (mESCs), chemical blockade of Gsk3α/β and Mek1/2 (2i) instructs a self-renewing ground state whose endogenous inducers are unknown. Here we show that the axon guidance cue Netrin-1 promotes naive pluripotency by triggering profound signalling, transcriptomic and epigenetic changes in mESCs. Furthermore, we demonstrate that Netrin-1 can substitute for blockade of Gsk3α/β and Mek1/2 to sustain self-renewal of mESCs in combination with leukaemia inhibitory factor and regulates the formation of the mouse pluripotent blastocyst. Mechanistically, we reveal how Netrin-1 and the balance of its receptors Neo1 and Unc5B co-regulate Wnt and MAPK pathways in both mouse and human ESCs. Netrin-1 induces Fak kinase to inactivate Gsk3α/β and stabilize β-catenin while increasing the phosphatase activity of a Ppp2r2c-containing Pp2a complex to reduce Erk1/2 activity. Collectively, this work identifies Netrin-1 as a regulator of pluripotency and reveals that it mediates different effects in mESCs depending on its receptor dosage, opening perspectives for balancing self-renewal and lineage commitment.
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