Unfolded protein response genes regulated by CED-1 are required for Caenorhabditis elegans innate immunity

被引：66

作者：

Haskins, Kylie A. ^{[1
]}

Russell, Jonathan F. ^{[1
]}

Gaddis, Nathan ^{[1
]}

Dressman, Holly K. ^{[1
,2
]}

Aballay, Alejandro ^{[1
]}

机构：

[1] Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC 27710 USA

[2] Duke Univ, Inst Genome Sci & Policy, Durham, NC 27708 USA

来源：

DEVELOPMENTAL CELL | 2008年 / 15卷 / 01期

关键词：

D O I：

10.1016/j.devcel.2008.05.006

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The endoplasmic reticulum stress response, also known as the unfolded protein response (UPR), has been implicated in the normal physiology of immune defense and in several disorders, including diabetes, cancer, and neurodegenerative disease. Here, we show that the apoptotic receptor CED-1 and a network of PQN/ABU proteins involved in a noncanonical UPR response are required for proper defense to pathogen infection in Caenorhabditis elegans. A full-genome microarray analysis indicates that CED-1 functions to activate the expression of pqn/abu genes. We also show that ced-1 and pqn/abu genes are required for the survival of C. elegans exposed to live Salmonella enterica, and that overexpression of pqn/abu genes confers protection against pathogen-mediated killing. The results indicate that unfolded protein response genes, regulated in a CED-1-dependent manner, are involved in the C. elegans immune response to live bacteria.

引用

页码：87 / 97

页数：11

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