Reptin and pontin antagonistically regulate heart growth in zebrafish embryos
Reptin and pontin antagonistically regulate heart growth in zebrafish embryos
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DOI：
10.1016/s0092-8674(02)01112-1
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发表时间：
2002-11-27
期刊：
影响因子：
64.5
通讯作者：
Fishman, M
中科院分区：
文献类型：
--
作者：
Rottbauer, W;Saurin, AJ;Fishman, M
器官的大小在发育过程中得到了精确的调节，但控制机制仍然不清楚。我们在斑马鱼中分离出了一种突变，liebetkummer(Lik)，它会导致胚胎心脏的发育。Lik编码Reptin，Reptin是DNA刺激的ATPase复合体的一个组成部分。该突变激活了Reptin复合体的ATPase活性，并导致心肌细胞在祖细胞形成原始心管后开始细胞自主增殖。在心脏生长方面，β-连环素和桥蛋白，一种DNA刺激的ATPase，通常是Reptin复合体的一部分，处于相同的遗传途径。Pontin减少性表现为Lik突变的心脏增生症。因此，Reptin/Pontin的比例至少部分通过β-连环蛋白途径，在发育过程中调节心脏的生长。
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.