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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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Citation

Rottbauer, W., Saurin, A. J., Lickert, H., Shen, X., Burns, C. G., Wo, Z. G., et al. (2002). Reptin and Pontin Antagonistically Regulate Heart Growth in Zebrafish Embryos. Cell, 111(5), 661-672.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-95E1-0
Abstract
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.