Community Action Needed: Please respond to the NIH RFI
ZFIN ID: ZDB-PUB-100317-6
Noncanonical Activity of Seryl-Transfer RNA Synthetase and Vascular Development
Kawahara, A., and Stainier, D.Y.
Date: 2009
Source: Trends in cardiovascular medicine   19(6): 179-182 (Review)
Registered Authors: Kawahara, Atsuo, Stainier, Didier
Keywords: none
MeSH Terms:
  • Animals
  • Blood Vessels/embryology
  • Blood Vessels/enzymology*
  • Gene Expression Regulation, Developmental
  • Humans
  • Morphogenesis
  • Mutation
  • Neovascularization, Physiologic*/genetics
  • Serine-tRNA Ligase/genetics
  • Serine-tRNA Ligase/metabolism*
  • Signal Transduction*/genetics
  • 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: 20211432 Full text @ Trends Cardiovasc. Med.
Seryl-transfer RNA synthetase (Sars) is one of the 20 aminoacyl-transfer RNA synthetases that are enzymes essential for protein synthesis; however, the developmental function of Sars has not been elucidated. In zebrafish, impairment of zygotic Sars function leads to a significant dilatation of the aortic arch vessels and aberrant branching of cranial and intersegmental vessels. This abnormal vascular branching in sars mutants can be suppressed by a form of Sars that lacks canonical function, indicating that a noncanonical activity of Sars regulates vascular development. Inhibition or knockdown of vascular endothelial growth factor (Vegf) signaling, which plays pivotal roles in the establishment of the vascular network, suppresses the abnormal vascular branching observed in sars mutants. Here, we discuss the possible functional relationship between Sars function and Vegf signaling.