Oral-aboral axis specification in the sea urchin embryo III. Role of mitochondrial redox signaling via H2O2.
Oral-aboral axis specification in the sea urchin embryo III. Role of mitochondrial redox signaling via H2O2.
复制标题
海胆胚胎III中的口腔宽轴规范。线粒体氧化还原信号通过H2O2的作用。
DOI：
10.1016/j.ydbio.2009.03.017
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发表时间：
2009-06-01
影响因子：
2.7
通讯作者：
Robertson, Anthony J.
中科院分区：
文献类型：
--
作者：
Coffman, James A.;Coluccio, Alison;Planchart, Antonio;Robertson, Anthony J.
在海胆胚胎中，次级(口腔-流产)轴的指定是通过节状发生的，其表达完全是合子的，并定位于囊胚期预期的口腔外胚层。这种空间各向异性的初始来源尚不清楚。先前的研究表明，口-胎(OA)的极性与线粒体的梯度有关，而结节的活动既依赖于线粒体的呼吸，也依赖于p38应激激活的蛋白激酶。在这里，我们表明，结节活动的空间模式也与线粒体梯度相关，后者与细胞内活性氧物种的不均匀水平相关。为了测试线粒体过氧化氢是否作为氧化还原信号激活结节，受精卵被注射了编码线粒体靶向过氧化氢酶和超氧化物歧化酶的mRNA，前者抑制线粒体过氧化氢并下调p38，后者增加线粒体过氧化氢并上调p38。前者通过2-细胞期卵裂球注射限制在胚胎的一半时，抑制了结节的初始激活，并将OA的极性带向流产，而后者不会产生相反的效果。我们得出结论，线粒体过氧化氢对结节的初始激活是限速的，但额外的限速因子可能也涉及线粒体，导致结节表达的不对称性。
In sea urchin embryos, specification of the secondary (oral-aboral) axis occurs via nodal, expression of which is entirely zygotic and localized to prospective oral ectoderm at blastula stage. The initial source of this spatial anisotropy is not known. Previous studies have shown that oral-aboral (OA) polarity correlates with a mitochondrial gradient, and that nodal activity is dependent both on mitochondrial respiration and p38 stress activated protein kinase. Here we show that the spatial pattern of nodal activity also correlates with the mitochondrial gradient, and that the latter correlates with inhomogeneous levels of intracellular reactive oxygen species. To test whether mitochondrial H2O2 functions as a redox signal to activate nodal, zygotes were injected with mRNA encoding either mitochondrially-targeted catalase, which quenches mitochondrial H2O2 and down-regulates p38, or superoxide dismutase, which augments mitochondrial H2O2 and up-regulates p38. Whereas the former treatment inhibits the initial activation of nodal and entrains OA polarity toward aboral when confined to half of the embryo via 2-cell stage blastomere injections, the latter does not produce the opposite effects. We conclude that mitochondrial H2O2 is rate-limiting for the initial activation of nodal, but that additional rate-limiting factors, likely also involving mitochondria, contribute to the asymmetry in nodal expression.
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