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ETV2-ECSCR-mTOR pathways regulate reprogramming to the endothelial lineage.

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ETV2 drives cell reprogramming, but its target Ecscr acts as a brake. Suppressing Ecscr enhances endothelial cell reprogramming by modulating mTORC1 signaling, offering new avenues for regenerative medicine.

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Regenerative Medicine

Background:

  • ETV2 is a crucial transcription factor for endothelial cell fate and reprogramming.
  • Downstream targets of ETV2 play a role in its cell fate-driving function.
  • Understanding ETV2's regulatory network is key to improving reprogramming efficiency.

Purpose of the Study:

  • To identify and characterize novel downstream targets of ETV2 involved in cell reprogramming.
  • To elucidate the functional role of Ecscr in ETV2-mediated endothelial cell fate conversion.
  • To explore the mechanistic basis of Ecscr's regulation and its impact on reprogramming.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) on ETV2-overexpressing systems.
  • Chromatin accessibility (ATAC-seq) and immunoprecipitation (ChIP-seq) assays.
  • In vivo studies using reporter mice and knockout models, gene knockdown, and pharmacological inhibition.

Main Results:

  • Ecscr was identified as a direct transcriptional target of ETV2, upregulated during reprogramming.
  • Ecscr knockdown enhanced ETV2-driven reprogramming efficiency, indicating a feedback inhibitory role.
  • Ecscr regulates reprogramming via the mTORC1 signaling pathway, with Rptor upregulation observed upon Ecscr knockdown.

Conclusions:

  • Ecscr is a novel ETV2 downstream target that negatively modulates endothelial reprogramming.
  • The ETV2-Ecscr axis influences cell fate through mTORC1 signaling.
  • Targeting Ecscr and mTORC1 offers potential strategies to enhance endothelial reprogramming for regenerative medicine.