Evolution of the fish heart by sub/neofunctionalization of an elastin gene
Yuuta Moriyama (),
Fumihiro Ito,
Hiroyuki Takeda,
Tohru Yano,
Masataka Okabe,
Shigehiro Kuraku,
Fred W. Keeley and
Kazuko Koshiba-Takeuchi ()
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Yuuta Moriyama: Institute of Molecular and Cellular Biosciences, The University of Tokyo
Fumihiro Ito: National Institute of Genetics
Hiroyuki Takeda: Graduate School of Science, The University of Tokyo
Tohru Yano: The Jikei University School of Medicine
Masataka Okabe: The Jikei University School of Medicine
Shigehiro Kuraku: Phyloinformatics Unit, RIKEN Center for Life Science Technologies
Fred W. Keeley: Research Institute, The Hospital for Sick Children
Kazuko Koshiba-Takeuchi: Institute of Molecular and Cellular Biosciences, The University of Tokyo
Nature Communications, 2016, vol. 7, issue 1, 1-10
Abstract:
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.
Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10397
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DOI: 10.1038/ncomms10397
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