
ERK 신호 전달은 naive 상태 유지 네트워크를 해체하고 formative 상태로의 진입을 보장하는 데 필수적이다.


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Naïve epiblast cells in the embryo and pluripotent stem cells in vitro undergo developmental progression to a formative state competent for lineage specification. During this transition, transcription factors and chromatin are rewired to encode new functional features. Here, we examine the role of mitogen-activated protein kinase (ERK1/2) signalling in pluripotent state transition. We show that a primary consequence of ERK activation in mouse embryonic stem cells is elimination of Nanog, precipitating breakdown of the naïve state gene regulatory network. Cell variability in pERK dynamics results in metachronous down-regulation of Nanog and naïve state exit. Knockdown of Nanog allows exit without ERK activation. However, transition to formative pluripotency does not proceed and cells collapse to an indeterminate identity. This failure is attributable to loss of expression of the central pluripotency factor Oct4. Thus, during formative transition ERK signalling both dismantles the naïve state and preserves pluripotency. These results illustrate that a single signalling pathway can both drive exit from a developmental state and safeguard progression to the successor state.

### Competing Interest Statement

The authors have declared no competing interest.

ERK signalling orchestrates metachronous transition from naïve to formative pluripotency

erk-신호-전달이-naive에서-formative-다능성으로의-시간차-있는-전환을-조율한다


ERK 신호 전달이 naive에서 formative 다능성으로의 시간차 있는 전환을 조율한다
