Plasticity of the inner cell mass in mouse blastocyst is restricted by the activity of FGF/MAPK pathway.
Plasticity of the inner cell mass in mouse blastocyst is restricted by the activity of FGF/MAPK pathway.
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DOI：
10.1038/s41598-017-15427-0
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发表时间：
2017-11-09
影响因子：
4.6
通讯作者：
Suwińska A
中科院分区：
文献类型：
--
作者：
Wigger M;Kisielewska K;Filimonow K;Plusa B;Maleszewski M;Suwińska A
为了确保成功的发育，早期哺乳动物胚胎的细胞必须分化为滋养外胚层（TE）或内细胞团（ICM），然后在ICM内分化为上胚层（EPI）或原始内胚层（PE）。在这里，我们破译了确保这些连续细胞命运决定的正确顺序的机制。我们发现，TE剥夺ICM来自32细胞囊胚仍然能够重建TE在体外培养过程中，证实了在这个阶段的ICM细胞的全能性。从更高级的囊胚中分离的ICM不再保持全能性，不能形成TE并在其表面产生PE。我们证明了从完全效力到谱系引发的转变是通过抑制FGF/MAPK信号通路来阻止的。此外，我们发现，在第一个限制步骤之后，ICM细胞仍然保持命运灵活性，表现为能够将其命运转化为替代谱系（PE朝向EPI，反之亦然），直到围着床期。
In order to ensure successful development, cells of the early mammalian embryo must differentiate to either trophectoderm (TE) or inner cell mass (ICM), followed by epiblast (EPI) or primitive endoderm (PE) specification within the ICM. Here, we deciphered the mechanism that assures the correct order of these sequential cell fate decisions. We revealed that TE-deprived ICMs derived from 32-cell blastocysts are still able to reconstruct TE during in vitro culture, confirming totipotency of ICM cells at this stage. ICMs isolated from more advanced blastocysts no longer retain totipotency, failing to form TE and generating PE on their surface. We demonstrated that the transition from full potency to lineage priming is prevented by inhibition of the FGF/MAPK signalling pathway. Moreover, we found that after this first restriction step, ICM cells still retain fate flexibility, manifested by ability to convert their fate into an alternative lineage (PE towards EPI and vice versa), until peri-implantation stage.
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