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首页> 外文期刊>Development >JAK/STAT signaling promotes regional specification by negatively regulating wingless expression in Drosophila.
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JAK/STAT signaling promotes regional specification by negatively regulating wingless expression in Drosophila.

机译：JAK / STAT信号传导通过负调节果蝇中的无翅表达来促进区域规范。

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During development, a small number of conserved signaling molecules regulate regional specification, in which uniform populations of cells acquire differences and ultimately give rise to distinct organs. In the Drosophila eye imaginal disc, Wingless (Wg) signaling defines the region that gives rise to head tissue. JAK/STAT signaling was thought to regulate growth of the eye disc but not pattern formation. However, we show that the JAK/STAT pathway plays an important role in patterning the eye disc: it promotes formation of the eye field through repression of the wg gene. Overexpression of the JAK/STAT activating ligand Unpaired in the eye leads to loss of wg expression and ectopic morphogenetic furrow initiation from the lateral margins. Conversely, tissue lacking stat92E, which cannot transduce JAK/STAT signals, is transformed from retinal tissue into head cuticle, a phenotype that is also observed with ectopic Wg signaling. Consistent with this, cells lacking stat92E exhibit ectopic wg expression. Conversely, wg is autonomously repressed in cells with hyperactivated Stat92E. Furthermore, we show that the JAK/STAT pathway regulates a small enhancer in the wg 3' cis genomic region. As this enhancer is devoid of Stat92E-binding elements, we conclude that Stat92E represses wg through another, as yet unidentified factor that is probably a direct target of Stat92E. Taken together, our study is the first to demonstrate a role for the JAK/STAT pathway in regional specification by acting antagonistically to wg.
机译：在发育过程中，少数保守的信号分子调节区域规格，其中均匀的细胞群获得差异并最终产生不同的器官。在果蝇眼假想盘中，无翅（Wg）信号定义了引起头部组织的区域。人们认为JAK / STAT信号传导可调节眼球的生长，但不能调节眼球的形成。但是，我们表明，JAK / STAT通路在图案化眼球方面起着重要作用：它通过抑制wg基因促进了视野的形成。 JAK / STAT激活配体的过度表达在眼睛中未成对会导致wg表达的丧失和从外侧边缘开始的异位形态发生沟。相反，缺乏stat92E的组织不能转导JAK / STAT信号，则从视网膜组织转变为头部角质层，这种表型在异位Wg信号传导中也观察到。与此一致，缺乏stat92E的细胞表现出异位wg表达。相反，wg在具有高度激活的Stat92E的细胞中被自主抑制。此外，我们表明，JAK / STAT通路调节wg 3'顺式基因组区域中的一个小的增强子。由于该增强子不含Stat92E结合元件，因此我们得出结论，Stat92E通过另一个尚未确定的因素抑制wg，这可能是Stat92E的直接靶标。两者合计，我们的研究是第一个通过拮抗wg来证明JAK / STAT途径在区域规范中的作用的研究。

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