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Abi induces ectopic sensory organ formation by stimulating EGFR signaling

机译:Abi通过刺激EGFR信号传导诱导异位感觉器官形成

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One of the central regulators coupling tyrosine phosphorylation with cytoskeletal dynamics is the Abelson interactor (Abi). Its activity regulates WASP-/WAVE mediated F-actin formation and in addition modulates the activity of the Abelson tyrosine kinase (Abl). We have recently shown that the Drosophila Abi is capable of promoting bristle development in a wasp dependent fashion. Here, we report that Drosophila Abi induces sensory organ development by modulating EGFR signaling. Expression of a membrane-tethered activated Abi protein (Abi(Myr)) leads to an increase in MAPK activity. Additionally, suppression of EGFR activity inhibits the induction of extra-sensory organs by Abi(Myr), whereas co-expression of activated Abi(Myr) and EGFR dramatically enhances the neurogenic phenotype. In agreement with this observation Abi is able to associate with the EGFR in a common complex. Furthermore, Abi binds the Abl tyrosine kinase. A block of Abl kinase-activity reduces Abi protein stability and strongly abrogates ectopic sensory organ formation induced by Abi(Myr). Concomitantly, we noted changes in tyrosine phosphorylation supporting previous reports that Abi protein stability is linked to tyrosine phosphorylation mediated by Abl.
机译:酪氨酸磷酸化与细胞骨架动力学耦合的中央调节剂之一是Abelson相互作用子(Abi)。它的活性调节WASP- / WAVE介导的F-肌动蛋白的形成,此外还调节Abelson酪氨酸激酶(Abl)的活性。我们最近表明,果蝇Abi能够以依赖于黄蜂的方式促进猪鬃的发育。在这里,我们报告果蝇Abi通过调节EGFR信号传导诱导感觉器官发育。膜束缚的活化Abi蛋白(Abi(Myr))的表达导致MAPK活性增加。此外,EGFR活性的抑制会抑制Abi(Myr)对超感觉器官的诱导,而活化Abi(Myr)和EGFR的共表达会显着增强神经源性表型。与该观察结果一致,Abi能够与EGFR缔合,形成共同的复合体。此外,Abi结合Abl酪氨酸激酶。阻止Abl激酶活性降低Abi蛋白的稳定性,并强力消除Abi(Myr)诱导的异位感觉器官的形成。同时,我们注意到酪氨酸磷酸化的变化支持以前的报道,即Abi蛋白的稳定性与Abl介导的酪氨酸磷酸化有关。

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