A mutation in the zebrafish Na,K-ATPase subunit atp1a1a.1 provides genetic evidence that the sodium potassium pump contributes to left-right asymmetry downstream or in parallel to Nodal flow
A mutation in the zebrafish Na,K-ATPase subunit atp1a1a.1 provides genetic evidence that the sodium potassium pump contributes to left-right asymmetry downstream or in parallel to Nodal flow
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DOI：
10.1002/dvdy.20800
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发表时间：
2006-07-01
影响因子：
2.5
通讯作者：
Driever, Wolfgang
中科院分区：
文献类型：
--
作者：
Ellertsdottir, Elin;Ganz, Julia;Driever, Wolfgang
虽然在大多数脊椎动物群体中有一个很好的背腹轴和前后轴形成的概念框架，但对左右轴起始的理解是零散的。不同的机制被认为是导致左右不对称的最早的机制，包括小分子信号、缝隙连接通讯、膜电位以及由单纤毛在结节区域产生的细胞外液的定向流动。在这里，我们证明了斑马鱼Na，K-ATPase亚单位atp1a1a的突变导致了从左到右的缺陷，包括解剖水平上的内脏异构性。正常左侧的结节信号Spaw及其抑制物Lefty呈双侧表达，而Pitx2可能表现为随机或双侧表达。在atp1a1a(M883)突变胚胎中，库普弗氏囊泡的单丝运动和液体循环是正常的。因此，在斑马鱼启动左右不对称的过程中，Na，K-ATPase需要下游或平行于单丝功能。
While there is a good conceptual framework of dorsoventral and anterioposterior axes formation in most vertebrate groups, understanding of left-right axis initiation is fragmentary. Diverse mechanisms have been implied to contribute to the earliest steps of left-right asymmetry, including small molecule signals, gap junctional communication, membrane potential, and directional flow of extracellular liquid generated by monocilia in the node region. Here we demonstrate that a mutation in the zebrafish Na,K-ATPase subunit atp1a1a causes left-right defects including isomerism of internal organs at the anatomical level. The normally left-sided Nodal signal spaw as well as its inhibitor lefty are expressed bilaterally, while pitx2 may appear random or bilateral. Monocilia movement and fluid circulation in Kupffer's vesicle are normal in atp1a1a(m883) mutant embryos. Therefore, the Na,K-ATPase is required downstream or in parallel to monocilia function during initiation of left-right asymmetry in zebrafish.