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首页> 外文期刊>Molecular and Cellular Biology >Discrete Functions of TRAF1 and TRAF2 in Drosophila melanogaster Mediated by c-Jun N-Terminal Kinase and NF-κB-Dependent Signaling Pathways
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Discrete Functions of TRAF1 and TRAF2 in Drosophila melanogaster Mediated by c-Jun N-Terminal Kinase and NF-κB-Dependent Signaling Pathways

机译：c-Jun N-末端激酶和依赖于NF-κB的信号通路介导的果蝇TRAF1和TRAF2的离散功能

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Two Drosophila tumor necrosis factor receptor-associated factors (TRAF), DTRAF1 and DTRAF2, are proposed to have similar functions with their mammalian counterparts as a signal mediator of cell surface receptors. However, their in vivo functions and related signaling pathways are not fully understood yet. Here, we show that DTRAF1 is an in vivo regulator of c-Jun N-terminal kinase (JNK) pathway in Drosophila melanogaster. Ectopic expression of DTRAF1 in the developing eye induced apoptosis, thereby causing a rough-eye phenotype. Further genetic interaction analyses revealed that the apoptosis in the eye imaginal disc and the abnormal eye morphogenesis induced by DTRAF1 are dependent on JNK and its upstream kinases, Hep and DTAK1. In support of these results, DTRAF1-null mutant showed a remarkable reduction in JNK activity with an impaired development of imaginal discs and a defective formation of photosensory neuron arrays. In contrast, DTRAF2 was demonstrated as an upstream activator of nuclear factor-κB (NF-κB). Ectopic expression of DTRAF2 induced nuclear translocation of two Drosophila NF-κBs, DIF and Relish, consequently activating the transcription of the antimicrobial peptide genes diptericin, diptericin-like protein, and drosomycin. Consistently, the null mutant of DTRAF2 showed immune deficiencies in which NF-κB nuclear translocation and antimicrobial gene transcription against microbial infection were severely impaired. Collectively, our findings demonstrate that DTRAF1 and DTRAF2 play pivotal roles in Drosophila development and innate immunity by differentially regulating the JNK- and the NF-κB-dependent signaling pathway, respectively.
机译：有人提出两个果蝇肿瘤坏死因子受体相关因子（TRAF）DTRAF1和DTRAF2具有与哺乳动物对应的类似功能，作为细胞表面受体的信号介质。但是，它们的体内功能和相关的信号通路尚不完全清楚。在这里，我们显示DTRAF1是果蝇果蝇中c-Jun N末端激酶（JNK）途径的体内调节剂。 DTRAF1在发育中的眼中异位表达可诱导细胞凋亡，从而引起粗糙的眼表型。进一步的遗传相互作用分析表明，DTRAF1诱导的眼球间盘凋亡和异常的眼形态发生取决于JNK及其上游激酶Hep和DTAK1。支持这些结果的是， DTRAF1 -null突变体显示JNK活性显着降低，并影响了视盘的发育，并损害了光敏神经元阵列的形成。相反，DTRAF2被证明是核因子-κB（NF-κB）的上游激活剂。 DTRAF2的异位表达诱导了两个果蝇NF-κB，DIF和Relish的核易位，因此激活了抗菌肽基因 diptericin ， diptericin-like蛋白的转录和 drosomycin 。一致地， DTRAF2 的无效突变体显示出免疫缺陷，其中严重破坏了NF-κB核转运和抗微生物感染的抗菌基因转录。总体而言，我们的研究结果表明DTRAF1和DTRAF2通过分别调节JNK和NF-κB依赖性信号通路在果蝇的发育和先天免疫中发挥关键作用。

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