4.8 Article

Endothelial versus pronephron fate decision is modulated by the transcription factors Cloche/Npas4l, Tal1, and Lmo2

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SCIENCE ADVANCES
卷 8, 期 35, 页码 -

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AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abn2082

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资金

  1. Max-Planck-Gesellschaft
  2. ERC [ZMOD 694455]
  3. Deutsche Forschungsgemeinschaft [BR 1746/6-1, BR 1746/6-2, BR 1746/3, SFB1213]
  4. University of Colorado School of Medicine
  5. Children's Hospital Colorado Foundation
  6. Swiss National Science Foundation [PP00P3_170623]
  7. TU Dresden
  8. Landes-Offensive zur Entwicklung Wissenschaftlich-okonomischer Exzellenz (LOEWE) of the State of Hessen, Research Center for Translational Biodiversity Genomics (TBG)
  9. ERC advanced grant (Zf-BrainReg)
  10. Cardio-Pulmonary Institute (CPI), Frankfurt, Germany
  11. Swiss National Science Foundation (SNF) [PP00P3_170623] Funding Source: Swiss National Science Foundation (SNF)

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This study reveals that Npas4l/Tal1/Lmo2 play a role in the fate decision between the endothelial and pronephron lineages. Npas4l induces the expression of the transcription factor genes etsrp, tall, and Imo2, which are crucial for endothelial specification.
Endothelial specification is a key event during embryogenesis; however, when, and how, endothelial cells separate from other lineages is poorly understood. In zebrafish, Npas4l is indispensable for endothelial specification by inducing the expression of the transcription factor genes etsrp, tall, and Imo2. We generated a knock-in reporter in zebrafish npas4l to visualize endothelial progenitors and their derivatives in wild-type and mutant embryos. Unexpectedly, we find that in npas4l mutants, npas4l reporter-expressing cells contribute to the pronephron tubules. Single-cell transcriptomics and live imaging of the early lateral plate mesoderm in wild-type embryos indeed reveals coexpression of endothelial and pronephron markers, a finding confirmed by creERT2-based lineage tracing. Increased contribution of npas4l reporter-expressing cells to pronephron tubules is also observed in tall and Imo2 mutants and is reversed in npas4l mutants injected with tall mRNA. Together, these data reveal that Npas4l/Tal1/Lmo2 regulate the fate decision between the endothelial and pronephron lineages.

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