C. elegans detects pathogen-induced translational inhibition to activate immune signaling.
C. elegans detects pathogen-induced translational inhibition to activate immune signaling.
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DOI：
10.1016/j.chom.2012.02.008
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发表时间：
2012-04-19
影响因子：
30.3
通讯作者：
Troemel ER
中科院分区：
文献类型：
--
作者：
Dunbar TL;Yan Z;Balla KM;Smelkinson MG;Troemel ER
Pathogens commonly disrupt host cell processes or cause damage, but the surveillance mechanisms used by animals to monitor these attacks are poorly understood. Upon infection with pathogenic Pseudomonas aeruginosa, the nematode C. elegans upregulates infection response gene irg-1 using the zip-2 bZIP transcription factor. Here we show that P. aeruginosa infection inhibits mRNA translation in the intestine via the endocytosed translation inhibitor Exotoxin A, which leads to an increase in ZIP-2 protein levels. In the absence of infection we find that the zip-2/irg-1 pathway is upregulated following disruption of several core host processes, including inhibition of mRNA translation. ZIP-2 induction is conferred by a conserved upstream open reading frame in zip-2 that could de-repress ZIP-2 translation upon infection. Thus, translational inhibition, a common pathogenic strategy, can trigger activation of an immune surveillance pathway to provide host defense.
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