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首页> 外文期刊>Current Biology: CB >C-elegans STAT cooperates with DAF-7/TGF-beta signaling to repress Dauer formation
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C-elegans STAT cooperates with DAF-7/TGF-beta signaling to repress Dauer formation

机译：C-线虫STAT与DAF-7 / TGF-beta信号传导共同抑制Dauer的形成

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The DAF-7/TGF-beta pathway in C. elegans interprets environmental signals relayed through amphid neurons and actively inhibits dauer formation during reproductive developmental growth [1, 2]. In metazoans, the STAT pathway interprets external stimuli through regulated tyrosine phosphorylation, nuclear translocation, and gene expression [3], but its importance for developmental commitment, particularly in conjuction with TGF-beta, remains largely unknown. Here, we report that the nematode STAT ortholog STA-1 accumulated in the nuclei of five head neuron pairs, three of which are amphid neurons involved in dauer formation [1, 4]. Moreover, sta-1 mutants showed a synthetic dauer phenotype with selected TGF-P mutations. sta-1 deficiency was complemented by reconstitution with wildtype protein, but not with a tyrosine mutant. Canonical TGF-beta signaling involves the DAF-7/TGF-beta ligand activating the DAF-1/DAF-4 receptor pair to regulate the DAF-8/DAF-14 Smads [5]. Interestingly, STA-1 functioned in the absence of DAF-7, DAF-4, and DAF-14, but it required DAF-1 and DAF-8. Additionally, STA-1 expression was induced by TGF-P in a DAF-3-dependent manner, demonstrating a homeostatic negative feedback loop. These results highlight a role for activated STAT proteins in repression of dauer formation. They also raise the possibility of an unexpected function for DAF-1 and DAF-8 that is independent of their normal upstream activator, DAF-7.
机译：秀丽隐杆线虫中的DAF-7 /TGF-β途径解释了通过两性神经元传递的环境信号，并在生殖发育生长过程中积极抑制了dauer的形成[1、2]。在后生动物中，STAT通路通过调节的酪氨酸磷酸化，核易位和基因表达来解释外部刺激[3]，但其对发育的重要性，特别是与TGF-β结合的重要性，仍是未知之数。在这里，我们报道线虫STAT直系同源物STA-1积累在五个头部神经元对的核中，其中三个是参与道尔形成的两性神经元[1，4]。此外，sta-1突变体显示具有选定的TGF-P突变的合成dauer表型。 sta-1缺乏症可以通过野生型蛋白的重组来补充，而不是酪氨酸突变体的重组。典型的TGF-β信号传导涉及激活DAF-1 / DAF-4受体对的DAF-7 /TGF-β配体，以调节DAF-8 / DAF-14 Smads [5]。有趣的是，STA-1在没有DAF-7，DAF-4和DAF-14的情况下起作用，但它需要DAF-1和DAF-8。另外，TGF-P以DAF-3依赖性的方式诱导STA-1表达，这表明体内负反馈回路。这些结果强调了活化的STAT蛋白在抑制dauer形成中的作用。它们还增加了DAF-1和DAF-8意外功能的可能性，这些功能独立于其正常的上游活化剂DAF-7。

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