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首页> 外文期刊>PLoS Genetics >A Novel Role for MAPKAPK2 in Morphogenesis during Zebrafish Development
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A Novel Role for MAPKAPK2 in Morphogenesis during Zebrafish Development

机译：MAPKAPK2在斑马鱼发育过程中的形态发生中的新作用。

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One of the earliest morphogenetic processes in the development of many animals is epiboly. In the zebrafish, epiboly ensues when the animally localized blastoderm cells spread, thin over, and enclose the vegetally localized yolk. Only a few factors are known to function in this fundamental process. We identified a maternal-effect mutant, betty boop (bbp), which displays a novel defect in epiboly, wherein the blastoderm margin constricts dramatically, precisely when half of the yolk cell is covered by the blastoderm, causing the yolk cell to burst. Whole-blastoderm transplants and mRNA microinjection rescue demonstrate that Bbp functions in the yolk cell to regulate epiboly. We positionally cloned the maternal-effect bbp mutant gene and identified it as the zebrafish homolog of the serine-threonine kinase Mitogen Activated Protein Kinase Activated Protein Kinase 2, or MAPKAPK2, which was not previously known to function in embryonic development. We show that the regulation of MAPKAPK2 is conserved and p38 MAP kinase functions upstream of MAPKAPK2 in regulating epiboly in the zebrafish embryo. Dramatic alterations in calcium dynamics, together with the massive marginal constrictive force observed in bbp mutants, indicate precocious constriction of an F-actin network within the yolk cell, which first forms at 50% epiboly and regulates epiboly progression. We show that MAPKAPK2 activity and its regulator p38 MAPK function in the yolk cell to regulate the process of epiboly, identifying a new pathway regulating this cell movement process. We postulate that a p38 MAPKAPK2 kinase cascade modulates the activity of F-actin at the yolk cell margin circumference allowing the gradual closure of the blastopore as epiboly progresses.
机译：外来是许多动物发育中最早的形态发生过程之一。在斑马鱼中，当动物定位的胚盘细胞散布，变薄并包围植物定位的蛋黄时，外表接着出现。在这一基本过程中，只有少数几个因素起作用。我们确定了一个母体效应突变体，贝蒂娃娃（bbp），它在表皮上显示出新的缺陷，其中胚盘边缘急剧收缩，恰好是当卵黄细胞的一半被胚盘覆盖时，卵黄细胞破裂。全胚层移植和mRNA显微注射抢救表明，Bbp在卵黄细胞中发挥功能来调节表皮。我们在位置上克隆了母本效应bbp突变基因，并将其鉴定为丝氨酸-苏氨酸激酶，丝裂素活化的蛋白激酶，活化的蛋白激酶2或MAPKAPK2的斑马鱼同源物，该蛋白以前在胚胎发育中不起作用。我们表明，MAPKAPK2的调节是保守的，p38 MAP激酶在调节斑马鱼胚胎的外突中在MAPKAPK2的上游起作用。钙动力学的剧烈变化，以及在bbp突变体中观察到的巨大边缘收缩力，表明卵黄细胞内F-肌动蛋白网络的早熟收缩，其首先在表皮的50％形成并调节表皮的发展。我们显示蛋黄细胞中的MAPKAPK2活性及其调节剂p38 MAPK功能调节表皮的过程，确定了调节该细胞运动过程的新途径。我们假设p38 MAPKAPK2激酶级联调节卵黄细胞边缘周围F-肌动蛋白的活性，使随着胚突的进展，胚孔逐渐闭合。

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