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.
Original language | English (US) |
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Pages (from-to) | 661-672 |
Number of pages | 12 |
Journal | Cell |
Volume | 111 |
Issue number | 5 |
DOIs | |
State | Published - Nov 27 2002 |
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology