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

  title={Long-Lived C. elegans daf-2 Mutants Are Resistant to Bacterial Pathogens},
  author={Danielle A. Garsin and Jacinto Villanueva and Jakob Begun and Dennis H. Kim and Costi D. Sifri and Stephen B. Calderwood and Gary Ruvkun and Frederick M. Ausubel},
  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 

Signaling in the immune response.

  • J. Ewbank
  • Biology
    WormBook : the online review of C. elegans biology
  • 2006
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.

C. elegans Germline-Deficient Mutants Respond to Pathogen Infection Using Shared and Distinct Mechanisms

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.

Expanding the nematode model system: The molecular basis of inflammation and infection recovery in C. elegans

The wholeorganism Caenorhabditis elegans-pathogen model is used to study the host recovery response from acute Pseudomonas aeruginosa infection and it is found that recovery was dependent on the GATA transcription factor elt-2 and the p38-mitogen-activated protein kinase (MAPK) pmk1.


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.

Innate immunity in C. elegans.

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.

DAF-16-Dependent Suppression of Immunity During Reproduction in Caenorhabditis elegans

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.

Insights from the worm: the C. elegans model for innate immunity.

Age influences resistance of Caenorhabditis elegans to killing by pathogenic bacteria.

Caenorhabditis elegans as a model for innate immunity to pathogens

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.



A Conserved p38 MAP Kinase Pathway in Caenorhabditis elegans Innate Immunity

RNA interference assays and biochemical analysis established that a p38 ortholog, pmk-1, functions as the downstream MAP kinase required for pathogen defense, suggesting that this MAP kinases signaling cassette represents an ancient feature of innate immune responses in evolutionarily diverse species.

Regulation of C. elegans life-span by insulinlike signaling in the nervous system.

Findings point to the nervous system as a central regulator of animal longevity by restoring daf-2 pathway signaling to muscle rescued metabolic defects, thus decoupling regulation of life-span and metabolism.

A simple model host for identifying Gram-positive virulence factors

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.

Genetics of aging.

The role of genetics in determining life-span is complex and paradoxical, and life-style and other environmental influences may profoundly modify outcomes of aging.

… genetics …

A possible genetic aetiology to CSVT, provides reliable risk estimates and allows accurate comparison with genetic risk in other vascular conditions is supported.

IL-13受体α2降低血吸虫病肉芽肿的炎症反应并延长宿主存活时间[英]/Mentink-Kane MM,Cheever AW,Thompson RW,et al//Proc Natl Acad Sci U S A


The difference in life-span between feeding on E. coli

    Annu. Rev. Genomics Hum. Genet

    • Annu. Rev. Genomics Hum. Genet
    • 2001