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首页> 外文期刊>Development >ERK- and JNK-signalling regulate gene networks that stimulate metamorphosis and apoptosis in tail tissues of ascidian tadpoles.
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ERK- and JNK-signalling regulate gene networks that stimulate metamorphosis and apoptosis in tail tissues of ascidian tadpoles.

机译:ERK和JNK信号调节基因网络刺激海cici尾部组织的变态和凋亡。

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摘要

In ascidian tadpoles, metamorphosis is triggered by a polarized wave of apoptosis, via mechanisms that are largely unknown. We demonstrate that the MAP kinases ERK and JNK are both required for the wave of apoptosis and metamorphosis. By employing a gene-profiling-based approach, we identified the network of genes controlled by either ERK or JNK activity that stimulate the onset of apoptosis. This approach identified a gene network involved in hormonal signalling, in innate immunity, in cell-cell communication and in the extracellular matrix. Through gene silencing, we show that Ci-sushi, a cell-cell communication protein controlled by JNK activity, is required for the wave of apoptosis that precedes tail regression. These observations lead us to propose a model of metamorphosis whereby JNK activity in the CNS induces apoptosis in several adjacent tissues that compose the tail by inducing the expression of genes such as Ci-sushi.
机译:在海ci中,通过细胞凋亡的极化波,通过很大程度上未知的机制触发了变态。我们证明MAP激酶ERK和JNK都是细胞凋亡和变态波所必需的。通过采用基于基因谱的方法,我们确定了由ERK或JNK活性控制的基因网络,该基因刺激了细胞凋亡的发作。这种方法确定了一个基因网络,该网络参与了激素信号传导,先天免疫,细胞间通讯以及细胞外基质。通过基因沉默,我们表明Ci-寿司,受JNK活性控制的细胞间通讯蛋白,是尾巴退化之前的细胞凋亡波所必需的。这些发现使我们提出了一种变态模型,其中CNS中的JNK活性通过诱导基因(例如Ci-sushi)的表达在组成尾巴的几个相邻组织中诱导凋亡。

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