The MAPKKK Mekk1 regulates the expression of Turandot stress genes in response to septic injury in Drosophila
The MAPKKK Mekk1 regulates the expression of Turandot stress genes in response to septic injury in Drosophila
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DOI：
10.1111/j.1365-2443.2006.00953.x
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发表时间：
2006-04-01
期刊：
影响因子：
2.1
通讯作者：
Lemaitre, B
中科院分区：
文献类型：
--
作者：
Brun, S;Vidal, S;Lemaitre, B
化脓性损伤会在果蝇成体中引发快速而广泛的反应，涉及对抗感染和伤口愈合所需的许多基因的上调。全基因组表达谱已经证明，这种反应是通过 Toll、Imd、JAK-STAT 和 JNK 途径的信号控制的。使用寡核苷酸微阵列，我们现在证明 MAPKKK Mekk1 调节脓毒症损伤诱导的一小部分基因，包括 Turandot (Tot) 应激基因。我们的分析表明，Tot 基因表现出复杂的调控模式，包括来自 JAK-STAT 和 Imd 途径以及 Mekk1 的信号。有趣的是，Mekk1 果蝇对微生物感染有抵抗力，但对氧化应激诱导剂百草枯敏感。这些结果表明 Mekk1 在防止组织损伤和/或蛋白质降解方面发挥着作用，并表明果蝇中应激和免疫途径之间存在复杂的相互作用。
Septic injury triggers a rapid and widespread response in Drosophila adults that involves the up-regulation of many genes required to combat infection and for wound healing. Genome-wide expression profiling has already demonstrated that this response is controlled by signaling through the Toll, Imd, JAK-STAT and JNK pathways. Using oligonucleotide microarrays, we now demonstrate that the MAPKKK Mekk1 regulates a small subset of genes induced by septic injury including Turandot (Tot) stress genes. Our analysis indicates that Tot genes show a complex regulation pattern including signals from both the JAK-STAT and Imd pathways and Mekk1. Interestingly, Mekk1 flies are resistant to microbial infection but susceptible to paraquat, an inducer of oxidative stress. These results point to a role of Mekk1 in the protection against tissue damage and/or protein degradation and indicate complex interactions between stress and immune pathways in Drosophila.