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Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila
eLife ( IF 6.4 ) Pub Date : 2020-01-16
Katrin Kierdorf, Fabian Hersperger, Jessica Sharrock, Crystal M Vincent, Pinar Ustaoglu, Jiawen Dou, Attila Gyoergy, Olaf Gross, Daria E Siekhaus, Marc S Dionne

Unpaired ligands are secreted signals that act via a GP130-like receptor, domeless, to activate JAK/STAT signaling in Drosophila. Like many mammalian cytokines, unpaireds can be activated by infection and other stresses and can promote insulin resistance in target tissues. However, the importance of this effect in non-inflammatory physiology is unknown. Here, we identify a requirement for unpaired-JAK signaling as a metabolic regulator in healthy adult Drosophila muscle. Adult muscles show basal JAK-STAT signaling activity in the absence of any immune challenge. Plasmatocytes (Drosophila macrophages) are an important source of this tonic signal. Loss of the dome receptor on adult muscles significantly reduces lifespan and causes local and systemic metabolic pathology. These pathologies result from hyperactivation of AKT and consequent deregulation of metabolism. Thus, we identify a cytokine signal that must be received in muscle to control AKT activity and metabolic homeostasis.

中文翻译:

肌肉功能和体内平衡需要细胞因子抑制果蝇中AKT活性

未配对的配体是通过GP130样受体(无圆顶)起作用的分泌信号,以激活果蝇中的JAK / STAT信号传导。像许多哺乳动物细胞因子一样,未配对可以被感染和其他压力激活,并可以促进靶组织中的胰岛素抵抗。然而,这种作用在非炎性生理学中的重要性尚不清楚。在这里,我们确定健康成年果蝇肌肉中不配对-JAK信号作为代谢调节剂的需求。在没有任何免疫攻击的情况下,成年肌肉显示出基础的JAK-STAT信号传导活性。浆细胞(果蝇巨噬细胞)是这种滋补信号的重要来源。的损失成年肌肉上的穹顶受体会显着缩短寿命,并引起局部和全身代谢病理。这些病理是由于AKT过度活化和随之而来的新陈代谢失调所致。因此,我们确定了必须在肌肉中接收以控制AKT活性和代谢稳态的细胞因子信号。
更新日期:2020-01-16
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