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

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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, tal1, and lmo2. 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 tal1 and lmo2 mutants and is reversed in npas4l mutants injected with tal1 mRNA. Together, these data reveal that Npas4l/Tal1/Lmo2 regulate the fate decision between the endothelial and pronephron lineages.


Original languageEnglish
Article numbereabn2082
Number of pages18
JournalScience advances
Issue number35
Publication statusPublished - 2 Sept 2022

External IDs

Scopus 85137048740
WOS 000879233400005
ORCID /0000-0003-0283-0211/work/142257347


Sustainable Development Goals

ASJC Scopus subject areas


  • Zebrafish gene cloche, Vascular development, Embryonic blood, Acts downstream, Protein rbtn2, Mesoderm, Kidney, Differentiation, Progenitors, Expression

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