PUBLICATION

Genetic duplication of tissue factor reveals subfunctionalization in venous and arterial hemostasis

Authors
Grzegorski, S.J., Zhao, Y., Richter, C.E., Ku, C.J., Lavik, K.I., Paul, D., Morrissey, J.H., Shavit, J.A.
ID
ZDB-PUB-221201-6
Date
2022
Source
PLoS Genetics   18: e1010534e1010534 (Journal)
Registered Authors
Grzegorski, Steven, Richter, Catherine, Shavit, Jordan, Zhao, Yakun
Keywords
none
MeSH Terms
  • Animals
  • Arteries/physiology
  • Gene Duplication*
  • Hemostasis*/genetics
  • Larva
  • Mice
  • Thromboplastin*/genetics
  • Thromboplastin*/physiology
  • Veins/physiology
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
PubMed
36449521 Full text @ PLoS Genet.
Abstract
Tissue factor (TF) is an evolutionarily conserved protein necessary for initiation of hemostasis. Zebrafish have two copies of the tissue factor gene (f3a and f3b) as the result of an ancestral teleost fish duplication event (so called ohnologs). In vivo physiologic studies of TF function have been difficult given early lethality of TF knockout in the mouse. We used genome editing to produce knockouts of both f3a and f3b in zebrafish. Since ohnologs arose through sub- or neofunctionalization, they can unmask unknown functions of non-teleost genes and could reveal whether mammalian TF has developmental functions distinct from coagulation. Here we show that a single copy of either f3a or f3b is necessary and sufficient for normal lifespan. Complete loss of TF results in lethal hemorrhage by 2-4 months despite normal embryonic and vascular development. Larval vascular endothelial injury reveals predominant roles for TFa in venous circulation and TFb in arterial circulation. Finally, we demonstrate that loss of TF predisposes to a stress-induced cardiac tamponade independent of its role in fibrin formation. Overall, our data suggest partial subfunctionalization of TFa and TFb. This multigenic zebrafish model has the potential to facilitate study of the role of TF in different vascular beds.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping