PUBLICATION

Akt is a mediator of artery specification during zebrafish development

Authors
Zhou, W., Ghersi, J.J., Ristori, E., Semanchik, N., Prendergast, A., Zhang, R., Carneiro, P., Baldissera, G., Sessa, W.C., Nicoli, S.
ID
ZDB-PUB-240806-2
Date
2024
Source
Development (Cambridge, England)   151(17): (Journal)
Registered Authors
Ghersi, Joey, Nicoli, Stefania, Prendergast, Andrew, Ristori, Emma
Keywords
Akt and Notch signaling, Artery specification, Endothelial cells, Single cell RNA sequencing., Vascular development, Zebrafish embryo
Datasets
GEO:GSE252648
MeSH Terms
  • Animals
  • Arteries*/embryology
  • Arteries*/metabolism
  • Embryo, Nonmammalian/metabolism
  • Endothelial Cells/metabolism
  • Gene Expression Regulation, Developmental
  • Mutation/genetics
  • Proto-Oncogene Proteins c-akt*/genetics
  • Proto-Oncogene Proteins c-akt*/metabolism
  • Receptors, Notch*/genetics
  • Receptors, Notch*/metabolism
  • Signal Transduction
  • Vascular Endothelial Growth Factor A/genetics
  • Vascular Endothelial Growth Factor A/metabolism
  • Zebrafish*/embryology
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
  • Zebrafish Proteins*/genetics
  • Zebrafish Proteins*/metabolism
PubMed
39101673 Full text @ Development
Abstract
The dorsal aorta (DA) is the first major blood vessel to develop in the embryonic cardiovascular system. Its formation is governed by a coordinated process involving the migration, specification, and arrangement of angioblasts into arterial and venous lineages, a process conserved across species. While vascular endothelial growth factor a (VEGF-A) drives DA specification and formation, the kinases involved in this process remain ambiguous. Thus, we investigated the role of protein kinase B, Akt, in zebrafish by generating a quadruple mutant (aktΔ/Δ), where expression and activity of all akt genes-akt 1, 2, 3a, and 3b are strongly decreased. Live imaging of developing aktΔ/Δ DA uncovers early arteriovenous malformations. Single-cell RNA sequencing analysis of aktΔ/Δ endothelial cells corroborates the impairment of arterial, yet not venous, cell specification. Notably, endothelial specific expression of ligand-independent activation of Notch or constitutively active Akt1 were sufficient to reestablish normal arterial specification in aktΔ/Δ. The Akt-loss-of-function mutant unveils that Akt kinase can act upstream of Notch in arterial endothelial cells, and is involved in proper embryonic artery specification. This sheds light on cardiovascular development, revealing a mechanism behind congenital malformations.
Genes / Markers
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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Mapping