Microbial pathogenesis and host defense in the nematode C. elegans

One contribution of 13 to a theme issue 'Evolutionary ecology of arthropod antimicrobial peptides'. Nematodes and arthropods likely form the taxon Ecdysozoa. Information on antimicrobial effectors from the model nematode Caenorhabditis elegans may thus shed light on the evolutionary origin of these defences in arthropods. This nematode species possesses an extensive armory of putative antimicrobial effector proteins, such as lysozymes, caenopores (or saposin-like proteins), defensin-like peptides, caenacins and neuropeptide-like proteins, in addition to the production of reactive oxygen species and autophagy. As C. elegans is a bacterivore that lives in microbe-rich environments, some of its effector peptides and proteins likely function in both digestion of bacterial food and pathogen elimination. In this review, we provide an overview of C. elegans immune effector proteins and mechanisms. We summarize the experimental evidence of their antimicrobial function and involvement in the response to pathogen infection. We further evaluate the microbe-induced expression of effector genes using WormExp, a recently established database for C. elegans gene expression analysis. We emphasize the need for further analysis at the protein level to demonstrate an antimicrobial activity of these molecules both in vitro and in vivo.This article is part of the themed issue 'Evolutionary ecology of arthropod antimicrobial peptides'.

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“…[13][14][15][16][17]). Thus, for the purpose of the current review, we only indicate some of the main elements.…”

Section: Brief Overview Of the Caenorhabditis Elegans Immune Systemmentioning

confidence: 99%

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

Dierking

Yang

Schulenburg

2016

Phil. Trans. R. Soc. B

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“…A relatively benign strain of E. coli is the typical C. elegans food source used experimentally, although its natural habitat contains a large number of species whose metabolic by-products are toxic to mitochondria [76]. These studies evolved from the finding that respiratory toxins produced by bacteria activate the UPR mt including the respiratory chain inhibitors antimycin and cyanide, and the ATP synthase inhibitor oligomycin [48, 49, 73].…”

Section: Protective Effects Mediated By the Uprmtmentioning

confidence: 99%

UPRmt-mediated cytoprotection and organismal aging

Schulz

Haynes

2015

Biochimica et Biophysica Acta (BBA) - Bioenergetics

102

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Time or age-dependent accumulation of mitochondrial damage and dysfunction is strongly associated with aging [1]. Thus, a major biomedical goal is to identify and therapeutically manipulate those inherent programs that protect against mitochondrial dysfunction to promote cell survival and organismal health. The mitochondrial unfolded protein response (UPRmt) is such a protective transcriptional response mediated by mitochondrial-to-nuclear signaling that includes mitochondrial proteostasis genes to stabilize mitochondrial function, metabolic adaptations, as well as an innate immunity program. Here, we review the UPRmt and its role during a variety of forms of mitochondrial dysfunction including those caused by mutations in respiratory chain genes as well as upon exposure to pathogens that produce mitochondrial toxins. We also review recent data in support of and against the emerging role of the UPRmt during aging and longevity.

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“…Bacterial toxins and secreted proteins, alter host mitochondrial function to promote pathogen proliferation and progression of infection [29][30][31][32] . As a consequence, mitochondria have developed protective mechanisms against pathogen invasion, including ROS generation 33 , inflammasome induction 34 , autophagy 31 and UPR mt activation 35 In addition to pronounced mitochondrial dysfunction, several bacterial species are known to induce UPR mt in nematodes, in the absence of other stressors 32,[35][36][37] . ATFS-1, the master regulator of UPR mt , is nuclearized in response to Pseudomonas aeruginosa infection and drives expression of several immune-response genes, including anti-microbial peptides and secreted lysozyme, similar to those induced by impairment of mitochondria function 35 .…”

Section: Mitochondrial Quality Control and Mitophagy: An Intricate Crmentioning

confidence: 99%

Interfacing mitochondrial biogenesis and elimination to enhance host pathogen defense and longevity

Palikaras

Lionaki

Tavernarakis

2015

Worm

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Mitochondria are highly dynamic and semi-autonomous organelles, essential for many fundamental cellular processes, including energy production, metabolite synthesis and calcium homeostasis, among others. Alterations in mitochondrial activity not only influence individual cell function but also, through non-cell autonomous mechanisms, whole body metabolism, healthspan and lifespan. Energy homeostasis is orchestrated by the complex interplay between mitochondrial biogenesis and mitochondria-selective autophagy (mitophagy). However, the cellular and molecular pathways that coordinate these 2 opposing processes remained obscure. In our recent study, we demonstrate that DCT-1, the Caenorhabditis elegans homolog of the mammalian BNIP3 and BNIP3L/NIX, is a key mediator of mitophagy, and functions in the same genetic pathway with PINK-1 and PDR-1 (the nematode homologs of PINK1 and Parkin respectively) to promote longevity and prevent cell damage under stress conditions. Interestingly, accumulation of damaged mitochondria activates SKN-1 (SKiNhead-1), the nematode homolog of NRF2, which in turn initiates a compensatory retrograde signaling response that impinges on both mitochondrial biogenesis and removal. In this commentary, we discuss the implications of these new findings in the context of innate immunity and aging. Unraveling the regulatory network that governs the crosstalk between mitochondrial biogenesis and mitophagy will enhance our understanding of the molecular mechanisms that link aberrant energy metabolism to aging and disease.

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Microbial pathogenesis and host defense in the nematode C. elegans

Cited by 87 publications

References 65 publications

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

UPRmt-mediated cytoprotection and organismal aging

Interfacing mitochondrial biogenesis and elimination to enhance host pathogen defense and longevity

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