Activation of Drosophila Toll during fungal infection by a blood serine protease

Activation of Drosophila Toll during fungal infection by a blood serine protease
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DOI:
10.1126/science.1072391
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发表时间:
2002-07-05
期刊:
影响因子:
56.9
通讯作者:
Reichhart, JM
Reichhart, JM
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Ligoxygakis, P;Pelte, N;Reichhart, JM

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果蝇对真菌和革兰氏阳性细菌感染的防御是由Spaetzle/Toll/cactus基因盒介导的。有人提出Toll本身并不是一种模式识别受体,而是通过细胞因子Spaetzle的裂解形式激活的。将感染与spetzle裂解联系起来的上游事件长期以来一直难以捉摸。在这里,我们报告了真菌激活Toll的一个核心组成部分的鉴定。我们发现乙基甲烷磺酸诱导的Persephone基因突变(编码一种以前未知的丝氨酸蛋白酶)阻断了真菌对Toll通路的诱导和对这种感染的抗性。
Drosophila host defense to fungal and Gram-positive bacterial infection is mediated by the Spaetzle/Toll/cactus gene cassette. It has been proposed that Toll does not function as a pattern recognition receptor per se but is activated through a cleaved form of the cytokine Spaetzle. The upstream events linking infection to the cleavage of Spaetzle have long remained elusive. Here we report the identification of a central component of the fungal activation of Toll. We show that ethylmethane sulfonate- induced mutations in the Persephone gene, which encodes a previously unknown serine protease, block induction of the Toll pathway by fungi and resistance to this type of infection.