Long-Lived C. elegans daf-2 Mutants Are Resistant to Bacterial Pathogens

@article{Garsin2003LongLivedCE,
  title={Long-Lived C. elegans daf-2 Mutants Are Resistant to Bacterial Pathogens},
  author={D. Garsin and J. Villanueva and J. Begun and Dennis H. Kim and C. Sifri and S. Calderwood and G. Ruvkun and F. Ausubel},
  journal={Science},
  year={2003},
  volume={300},
  pages={1921 - 1921}
}
Our laboratories have studied the mechanisms of aging ( [1][1], [2][2] ) and immune function ( [3][3] ) in Caenorhabditis elegans . Herein we show that the mechanisms that govern these two processes may be interrelated. The human Gram-negative bacterial pathogens Pseudomonas aeruginosa and 
Molecular mechanisms of resistance to human pathogenic bacteria in Caenorhabditis elegans by MEV-1 mediated oxidative stress.
TLDR
It is shown that mev-1RNAi causes a dramatic decrease in oxidative stress and antioxidant enzyme expressions, thereby leading to increased E. faecalis accumulation in nematode intestine, highlighting MEV-1 as a key regulatory component for determining genetic responsiveness to oxidant/antioxidant imbalance that is associated with innate immunity. Expand
Signaling in the immune response.
  • J. Ewbank
  • Biology, Medicine
  • WormBook : the online review of C. elegans biology
  • 2006
TLDR
This chapter describes the current understanding of the different innate immune responses of C. elegans that follow infection and focuses on the main signalling pathways that have been identified and highlights the inclusion of certain molecular cassettes in both immune and developmental functions. Expand
C. elegans Germline-Deficient Mutants Respond to Pathogen Infection Using Shared and Distinct Mechanisms
TLDR
It is shown that germline-deficient strains display increased resistance across a broad range of pathogens including Gram positive and Gram negative bacteria, and the fungal pathogen Cryptococcus neoformans, and that the FOXO transcription factor DAF-16, which regulates longevity and immunity in C. elegans, appears to be crucial for maintaining longevity in both wild-type and germline -deficient backgrounds. Expand
CHAPTER 6 INNATE IMMUNITY IN C . ELEGANS
The nematode Caenorhabditis elegans is proving to be a powerful invertebrate model to study host‐pathogen interactions. In common with other invertebrates, C. elegans relies solely on its innateExpand
Innate immunity in C. elegans.
TLDR
The current knowledge of the pathways and effector molecules involved in the nematode immune response, with a particular focus on the antifungal immune response of the C. elegans epidermis is summarized. Expand
DAF-16-Dependent Suppression of Immunity During Reproduction in Caenorhabditis elegans
TLDR
The timing of DAF-16-dependent gene activation in sterile mutants coincides with the onset of embryonic development in wild-type animals, suggesting that signals from developing embryos normally downregulate the immune response. Expand
Insights from the worm: the C. elegans model for innate immunity.
The nematode worm Caenorhabditis elegans comprises an ancestral immune system. C. elegans recognizes and responds to viral, bacterial, and fungal infections. Components of the RNA interferenceExpand
Age influences resistance of Caenorhabditis elegans to killing by pathogenic bacteria.
TLDR
It is shown that mutations in the age-1, and/or age-2 genes of C. elegans, that normally enhance life expectancy, can also increase resistance to killing by the bacterial pathogens Pseudomonas aeruginosa, Salmonella enterica var. Expand
Caenorhabditis elegans as a model for innate immunity to pathogens
TLDR
The discovery that the C. elegans worm has inducible defence responses, which to some extent parallel those of other organisms, demonstrates the potential of this model organism for the study of innate immunity. Expand
Bacterial Nitric Oxide Extends the Lifespan of C. elegans
TLDR
It is demonstrated that bacterially derived NO enhances C. elegans longevity and stress resistance via a defined group of genes that function under the dual control of HSF-1 and DAF-16 transcription factors. Expand
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It is shown here that infection of C. elegans by the Gram-negative bacterium Serratia marcescens provokes a marked upregulation of the expression of many genes, leading to the first demonstration of inducible antibacterial defenses in the nematode Caenorhabditis elegans. Expand
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TLDR
The use of the nematode Caenorhabditis elegans is demonstrated as a facile and inexpensive model host for several Gram-positive human bacterial pathogens and an E. faecalis virulence factor, ScrB, which is relevant to mammalian pathogenesis is exploited. Expand
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抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
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