PUBLICATION

Evolution of the fish heart by sub/neofunctionalization of an elastin gene

Authors
Moriyama, Y., Ito, F., Takeda, H., Yano, T., Okabe, M., Kuraku, S., Keeley, F.W., Koshiba-Takeuchi, K.
ID
ZDB-PUB-231218-21
Date
2016
Source
Nature communications   7: 1039710397 (Journal)
Registered Authors
Takeda, Hiroyuki, Yano, Tohru
Keywords
none
MeSH Terms
  • Animals
  • Elastin
  • Evolution, Molecular
  • Fish Proteins/genetics
  • Fish Proteins/metabolism
  • Fishes
  • Gene Duplication/genetics
  • Gene Duplication/physiology
  • Heart/physiology*
  • Muscle, Smooth/metabolism*
  • Myocardium/metabolism*
  • Phylogeny
PubMed
26783159 Full text @ Nat. Commun.
Abstract
The evolution of phenotypic traits is a key process in diversification of life. However, the mechanisms underlying the emergence of such evolutionary novelties are largely unknown. Here we address the origin of bulbus arteriosus (BA), an organ of evolutionary novelty seen in the teleost heart outflow tract (OFT), which sophisticates their circulatory system. The BA is a unique organ that is composed of smooth muscle while the OFTs in other vertebrates are composed of cardiac muscle. Here we reveal that the teleost-specific extracellular matrix (ECM) gene, elastin b, was generated by the teleost-specific whole-genome duplication and neofunctionalized to contribute to acquisition of the BA by regulating cell fate determination of cardiac precursor cells into smooth muscle. Furthermore, we show that the mechanotransducer yap is involved in this cell fate determination. Our findings reveal a mechanism of generating evolutionary novelty through alteration of cell fate determination by the ECM.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping