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Nat Commun. 2016 Jan 19;7:10397. doi: 10.1038/ncomms10397.

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

Author information

Division of Cardiovascular Regeneration, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo, Tokyo 113-0032, Japan.
Division of Ecological Genetics, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan.
Department of Genetics, The Graduate University for Advanced Studies (SOKENDAI), 1111 Yata, Mishima, Shizuoka 411-8540, Japan.
Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033, Japan.
Department of Anatomy, The Jikei University School of Medicine, 3-25-8 Nishishinbashi, Minato, Tokyo 105-8461, Japan.
Phyloinformatics Unit, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima-minamimachi, Chuo, Kobe, Hyogo 650-0047, Japan.
Research Institute, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada.
Department of Biochemistry, University of Toronto, Toronto, Ontario M5S 1A8, Canada.
Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba 277-8561, Japan.


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.

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