PUBLICATION

Tek/Tie2 is not required for cardiovascular development in zebrafish

Authors
Jiang, Z., Carlantoni, C., Allanki, S., Ebersberger, I., Stainier, D.Y.R.
ID
ZDB-PUB-201002-55
Date
2020
Source
Development (Cambridge, England)   147(19): (Journal)
Registered Authors
Stainier, Didier
Keywords
Cardiovascular development, Evolutionary genetics, Functional diversification, Genome editing, Morpholino, Tek/Tie2
MeSH Terms
  • Animals
  • Cardiovascular System/cytology
  • Cardiovascular System/metabolism*
  • Gene Editing
  • Organogenesis/genetics
  • Organogenesis/physiology
  • Phylogeny
  • Receptor, TIE-2/genetics
  • Receptor, TIE-2/metabolism
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
32928907 Full text @ Development
Abstract
Angiopoietin/TIE signalling plays a major role in blood and lymphatic vessel development. In mouse, Tek/Tie2 mutants die prenatally due to a severely underdeveloped cardiovascular system. In contrast, in zebrafish, previous studies have reported that while embryos injected with tek morpholinos (MOs) exhibit severe vascular defects, tek mutants display no obvious vascular malformations. To further investigate the function of zebrafish Tek, we generated a panel of loss-of-function tek mutants, including RNA-less alleles, an allele lacking the MO-binding site, an in-frame deletion allele, and a premature termination codon-containing allele. Our data show that all these mutants survive to adulthood with no obvious cardiovascular defects. MO injections into tek mutants lacking the MO-binding site or the entire tek locus cause similar vascular defects as those observed in MO-injected +/+ siblings, indicating off-target effects of the MOs. Surprisingly, comprehensive phylogenetic profiling and synteny analyses reveal that Tek was lost in the largest teleost clade, suggesting a lineage-specific shift in the function of TEK during vertebrate evolution. Altogether, these data show that Tek is dispensable for zebrafish development, and probably dispensable in most teleost species.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping