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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ca~(2+) channel-independent requirement for MAGUK family CACNB4 genes in initiation of zebrafish epiboly
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Ca~(2+) channel-independent requirement for MAGUK family CACNB4 genes in initiation of zebrafish epiboly

机译:Ca〜(2+)通道依赖性的斑马鱼表皮启动对MAGUK家族CACNB4基因的要求

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摘要

CACNB genes encode membrane-associated guanylate kinase (MAGUK) proteins once thought to function exclusively as auxiliary β subunits in assembly and gating of voltage-gated Ca~(2+) channels. Here, we report that zygotic deficiency of zebrafish β4 protein blocks initiation of epiboly, the first morphogenetic movement of teleost embryos. Reduced β4 function in the yolk syncytial layer (YSL) leads to abnormal division and dispersal of yolk syncytial nuclei, blastoderm retraction, and death, effects highly similar to microtubule disruption by nocodazole. Epiboly is restored by coinjection of human β4 cRNA or, surprisingly, by mutant cRNA encoding β4 subunits incapable of binding to Ca~(2+) channel α1 subunits. This study defines a YSL-driven zygotic mechanism essential for epiboly initiation and reveals a Ca~(2+) channel-independent β4 protein function potentially involving the cytoskeleton.
机译:CACNB基因编码膜相关的鸟苷酸激酶(MAGUK)蛋白,曾经被认为在电压门控Ca〜(2+)通道的组装和门控中仅作为辅助β亚基起作用。在这里,我们报道了斑马鱼β4蛋白的合子缺乏会阻止表皮的开始,这是硬骨鱼胚的第一个形态发生运动。卵黄合胞体层(YSL)中β4功能的降低会导致卵黄合胞体核的异常分裂和扩散,胚盘缩回和死亡,其作用与诺考达唑对微管的破坏高度相似。通过共注射人β4cRNA或通过令人惊讶的是,编码不能与Ca〜(2+)通道α1亚基结合的β4亚基的突变cRNA,恢复了表观抗体。这项研究定义了由YSL驱动的合子机制对于表皮启动至关重要,并揭示了Ca〜(2+)通道无关的β4蛋白功能,可能涉及细胞骨架。

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