Reptin and Pontin Antagonistically Regulate Heart Growth in Zebrafish Embryos

Rottbauer, Wolfgang; Saurin, Andrew J.; Lickert, Heiko; Shen, Xuetong; Burns, C. G.; Wo, Z. G.; Kemler, Rolf; Kingston, Robert; Wu, Carl; Fishman, Mark

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Reptin and Pontin Antagonistically Regulate Heart Growth in Zebrafish Embryos

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Lickert, Heiko
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Kemler, Rolf
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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引用

Rottbauer, W., Saurin, A. J., Lickert, H., Shen, X., Burns, C. G., Wo, Z. G., Kemler, R., Kingston, R., Wu, C., & Fishman, M. (2002). Reptin and Pontin Antagonistically Regulate Heart Growth in Zebrafish Embryos. Cell, 111(5), 661-672.

引用: https://hdl.handle.net/11858/00-001M-0000-002B-95E1-0

要旨

Organ size is precisely regulated during development, but the control mechanisms remain obscure. We have isolated a mutation in zebrafish, liebeskummer (lik), which causes development of hyperplastic embryonic hearts. lik encodes Reptin, a component of a DNA-stimulated ATPase complex. The mutation activates ATPase activity of Reptin complexes and causes a cell-autonomous proliferation of cardiomyocytes to begin well after progenitors have fashioned the primitive heart tube. With regard to heart growth, β-catenin and Pontin, a DNA-stimulated ATPase that is often part of complexes with Reptin, are in the same genetic pathways. Pontin reduction phenocopies the cardiac hyperplasia of the lik mutation. Thus, the Reptin/Pontin ratio serves to regulate heart growth during development, at least in part via the β-catenin pathway.