Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Virulence. 2012 May 1;3(3):238-40. doi: 10.4161/viru.20794.
The fungal pathogen Drechmeria coniospora infects C. elegans and elicits an innate immune response mediated, in part, by the induction of antimicrobial peptides in the epidermis. The signaling pathways controlling this phenomenon remain to be fully characterized. In this issue of Virulence, Couillault and colleagues use both proteomics and genetics to discover an unexpected role for the unfolded protein response (UPR) target chaperone BiP/GRP78/hsp-3 in the control of fungal infection-induced antimicrobial peptide expression in C. elegans. Although the expression of hsp-3 is regulated by the UPR, Couillault and colleagues describe a novel signaling role for this BiP/GRP78 homolog.
真菌病原体德雷切默里亚角孢菌感染秀丽隐杆线虫,并引发先天免疫反应,部分是通过表皮中抗菌肽的诱导介导的。控制这一现象的信号通路仍有待充分描述。在本期《毒力》杂志中,Couillault 及其同事利用蛋白质组学和遗传学发现了未折叠蛋白反应 (UPR) 靶伴侣蛋白 BiP/GRP78/hsp-3 在控制秀丽隐杆线虫真菌感染诱导抗菌肽表达中的意外作用。尽管 hsp-3 的表达受 UPR 调控,但 Couillault 及其同事描述了这种 BiP/GRP78 同源物的新的信号作用。