Journal
DEVELOPMENTAL CELL
Volume 15, Issue 1, Pages 87-97Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2008.05.006
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Funding
- NIAID NIH HHS [U54 AI057157] Funding Source: Medline
- NIGMS NIH HHS [R37 GM070977, R01 GM070977, R01 GM070977-01A1, GM070977] Funding Source: Medline
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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.
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