Ion flow regulates left-right asymmetry in sea urchin development
Ion flow regulates left-right asymmetry in sea urchin development
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DOI：
10.1007/s00427-005-0051-6
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发表时间：
2006-05-01
影响因子：
2.4
通讯作者：
Nishino, A
中科院分区：
文献类型：
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作者：
Hibino, T;Ishii, Y;Nishino, A
对左右（LR）轴模式的早期机制在门之间的保守程度知之甚少。海胆幼虫表现出一致的LR不对称性。成虫原基的主要部分由幼虫的左体腔囊即左水腔形成。虽然这种左偏好在所有棘皮动物幼虫中是保守的，但其机制在很大程度上还不清楚。使用两个标记基因，HpNot和HpFoxp 3样，这是不对称的海胆Hemicentrotus pulcherrimus的幼虫发育过程中表达的，我们在这项研究中研究的可能性，最近发现的离子通量机制控制不对称的海胆，因为它在几种脊椎动物物种。筛选了几种离子转运蛋白抑制剂，以确定其改变不对称标记基因表达的能力。H+/K+-ATP酶阻滞剂（奥美拉唑、兰索拉唑和SCH 28080）以及钙离子载体（A23187）显著改变了不对称基因表达的正常偏侧性。暴露于奥美拉唑破坏了幼虫成虫雏形形成的一致不对称性。免疫检测显示，海胆胚胎中的H+/K+-ATP酶样抗原贯穿囊胚期，并在32-细胞胚胎中表现出明显的不对称性，存在于单个卵裂球中。这些结果表明，在脊椎动物中，内源性空间调节的早期运输的H+和/或K+，也Ca 2+，在建立LR不对称海胆发展的功能。
The degree of conservation among phyla of early mechanisms that pattern the left - right (LR) axis is poorly understood. Larvae of sea urchins exhibit consistently oriented LR asymmetry. The main part of the adult rudiment is formed from the left coelomic sac of larvae, the left hydrocoel. Although this left preference is conserved among all echinoderm larvae, its mechanism is largely not understood. Using two marker genes, HpNot and HpFoxFQ-like, which are asymmetrically expressed during larval development of the sea urchin Hemicentrotus pulcherrimus, we examined in this study the possibility that the recently discovered ion flux mechanism controls asymmetry in sea urchins as it does in several vertebrate species. Several ion-transporter inhibitors were screened for the ability to alter the expression of the asymmetric marker genes. Blockers of the H+/K+-ATPase ( omeprazole, lansoprazole and SCH28080), as well as a calcium ionophore (A23187), significantly altered the normal sidedness of asymmetric gene expression. Exposure to omeprazole disrupted the consistent asymmetry of adult rudiment formation in larvae. Immuno-detection revealed that H+/K+-ATPase-like antigens in sea urchin embryos were present through blastula stage and exhibited a striking asymmetry being present in a single blastomere in 32-cell embryos. These results suggest that, as in vertebrates, endogenous spatially-regulated early transport of H+ and/or K+, and also of Ca2+, functions in the establishment of LR asymmetry in sea urchin development.