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PHD2 safeguards modest mesendoderm development
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DOI：10.1038/s42003-024-06824-z.png)
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Abstract
En 中文
PHD2 is essential in modulating HIF-1 alpha levels upon oxygen fluctuations. Hypoxia, a hallmark of uterus, and HIF-1 alpha have recently emerged as opposing regulators of mesendoderm specification, suggesting a role for PHD2 therein. We found that PHD2 expression initially covered the epiblast and gradually receded from the primitive streak, which was identical to hypoxia and exclusive to HIF-1 alpha. The investigations performed in mESCs, embryoids, and mouse embryos together demonstrated that PHD2 negatively regulated mesendoderm specification. Single-cell RNA sequencing revealed that PHD2 governed the transition from epiblast to mesendoderm. The downstream effect of PHD2 relied on the HIF-1 alpha regulated Wnt/beta-catenin pathway, while it was regulated upstream by miR-429. In summary, our research highlights PHD2's essential role in mesendoderm specification and its interactions with hypoxia and HIF-1 alpha. PHD2-mediated pseudohypoxia, rather than ambient hypoxia, safeguards a balanced mesendoderm specification, relying on the HIF1 alpha-regulated Wnt/beta-catenin pathway.
Keywords:
EMBRYONIC STEM-CELLS
HYPOXIA
DIFFERENTIATION
MIR-200
PREIMPLANTATION
OXYGEN
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