PUBLICATION
Reptin and pontin antagonistically regulate heart growth in zebrafish embryos
- Authors
- Rottbauer, W., Saurin, A.J., Lickert, H., Shen, X., Burns, C.G., Wo, Z.G., Kemler, R., Kingston, R., Wu, C., and Fishman, M.
- ID
- ZDB-PUB-021204-1
- Date
- 2002
- Source
- Cell 111(5): 661-672 (Journal)
- Registered Authors
- Fishman, Mark C., Rottbauer, Wolfgang
- Keywords
- none
- MeSH Terms
-
- Carrier Proteins
- Embryo, Nonmammalian
- Myocardium/cytology
- Myocardium/ultrastructure
- ATP-Dependent Proteases
- PubMed
- 12464178 Full text @ Cell
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, beta-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 beta-catenin pathway.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping