The G protein-coupled receptor FSHR-1 is required for the Caenorhabditis elegans innate immune response

被引:101
作者
Powell, Jennifer R. [1 ,2 ,3 ]
Kim, Dennis H. [1 ,2 ]
Ausubel, Frederick M. [1 ,2 ,3 ]
机构
[1] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA
[2] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA
[3] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA
基金
美国国家卫生研究院;
关键词
host-pathogen interactions; leucine-rich repeat; FOLLICLE-STIMULATING-HORMONE; TOLL-LIKE RECEPTOR; PATHWAY; RECOGNITION; ACTIVATION; RESISTANCE; DAF-16; SYSTEM; KINASE; GENES;
D O I
10.1073/pnas.0813048106
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Innate immunity is an ancient defense system used by both vertebrates and invertebrates. Previously characterized innate immune responses in plants and animals are triggered by detection of pathogens using specific receptors, which typically use a leucine-rich repeat (LRR) domain to bind molecular patterns associated with infection. The nematode Caenorhabditis elegans uses defense pathways conserved with vertebrates; however, the mechanism by which C. elegans detects pathogens is unknown. We screened all LRR-containing transmembrane receptors in C. elegans and identified the G protein-coupled receptor FSHR-1 as an important component of the C. elegans immune response to Gram-negative and Gram-positive bacterial pathogens. FSHR-1 acts in the C. elegans intestine, the primary site of exposure to ingested pathogens. FSHR-1 signals in parallel to the known p38 MAPK pathway but converges to regulate the transcriptional induction of an overlapping but nonidentical set of antimicrobial effectors. FSHR-1 may act generally to boost the nematode immune response, or it may function as a pathogen receptor.
引用
收藏
页码:2782 / 2787
页数:6
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