Life cycle of the endoparasitic nematophagous fungus Meria coniospora: a light and electron microscopic study

Jansson, Hans; Hofsten, Angelica V.; Mecklenburg, Claes von

doi:10.1007/bf00394645

Cited by 26 publications

(11 citation statements)

References 8 publications

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“…The actinomycete Streptomyces albireticuli and the fungus Drechmeria coniospora, natural pathogens of C. elegans , invade the gut epithelium (Jansson et al. ; Park et al. ).…”

Section: Discussionmentioning

confidence: 99%

The Caenorhabditis elegans p38 MAPK Gene plays a key role in protection from mycobacteria

et al. 2016

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Mitogen‐activated protein kinases (MAPK) are critical mediators of cellular responses to pathogens and are activated in response to infection, but investigation is difficult in multi‐cell hosts due to developmental lethality of mutations. Mycobacterium marinum (Mm) is an established model for tuberculosis, a disease afflicting nearly one‐third of the world's population. We found that Mm‐infected Caenorhabditis elegans display >80% mortality, but nonpathogenic M. smegmatis cause <15% mortality. C. elegans display pathological changes when infected with Mm, whereas Mm mutants produce lower mortality, suggesting that C. elegans is a promising virulence model for detailed genetic analysis. C. elegans MAPK mutants are hypersusceptible to mycobacterial infection; however, the C. elegans TOL‐like, TGF‐β and insulin‐like pathway genes do not play important roles in susceptibility. We show that pathogenic mycobacteria inhibit MAPK‐mediated protection through the MAPK phosphatase gene and demonstrate that C. elegans provide a genetically tractable pathogenicity model of both the host and pathogen.

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“…The actinomycete Streptomyces albireticuli and the fungus Drechmeria coniospora, natural pathogens of C. elegans , invade the gut epithelium (Jansson et al. ; Park et al. ).…”

Section: Discussionmentioning

confidence: 99%

The Caenorhabditis elegans p38 MAPK Gene plays a key role in protection from mycobacteria

et al. 2016

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“… 34,35 Its conidia (non-motile spores) can bind to the worm's cuticle through specialized adhesive knobs and upon germination spread hyphae throughout the worm's body, causing death after as little as 48 hours. 36 Some bacteria also adhere to the cuticle, like Leucobacter spp Verde 37 or Microbacterium nematophilum that colonizes the rectal cuticle and provokes swelling in the adjacent epithelia. 38,39 …”

Section: Pathogen Infectionmentioning

confidence: 99%

Mechanisms of innate immunity inC. elegansepidermis

Taffoni

Pujol

2015

Tissue Barriers

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The roundworm C. elegans has been successfully used for more than 50 y as a genetically tractable invertebrate model in diverse biological fields such as neurobiology, development and interactions. C. elegans feeds on bacteria and can be naturally infected by a wide range of microorganisms, including viruses, bacteria and fungi. Most of these pathogens infect C. elegans through its gut, but some have developed ways to infect the epidermis. In this review, we will mainly focus on epidermal innate immunity, in particular the signaling pathways and effectors activated upon wounding and fungal infection that serve to protect the host. We will discuss the parallels that exist between epidermal innate immune responses in nematodes and mammals.

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“…The overall mechanisms of the infection process were essentially similar to those described for the nematode P. redivivus, in particular with respect to the accumulation of lipid droplets inside trophic hyphae (Fig. la), the mode of conidiophore formation and the development and maturation of conidia [3,4,11].…”

Section: Infectionmentioning

confidence: 55%

“…After adhesion, an appressorium is formed on the knob which is shown to be a prerequisite for proper penetration of the prey [2,3]. Following penetration, infection proceeds, including colonization of the nematode body by trophic hyphae and formation of conidiophores and conidia outside the cuticle [4]. Within three days 100 percent of the nematodes are killed [5].…”

Section: Introductionmentioning

confidence: 99%

Conidia of the nematophagous fungus Drechmeria coniospora adhere to but barely infect Acrobeloides buetschilii

Dijksterhuis

Veenhuis

Harder

1993

FEMS Microbiology Letters

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Conidia of the endoparasitic fungus Drechmeria coniospora were able to adhere to the nematode Acrobeloides buetschilii; approximately 70% of the nematodes were carrying spores 16 h after their addition to the fungal culture. Young nematodes were preferentially affected; adhesion mainly took place in the head region of the animal. Full infection, characterized by colonization of the nematode body and production of conidiophores and conidia, was observed, albeit at low frequencies. In case of failure, a second adhesive knob was often formed on the germinated spore. The low frequencies of infection are not related to a loss of virulence, due to prolonged in vitro culturing of the fungus. Fresh spores, obtained from cultures which were passed several times through the host, did not show higher infection frequencies.

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Life cycle of the endoparasitic nematophagous fungus Meria coniospora: a light and electron microscopic study

Cited by 26 publications

References 8 publications

The Caenorhabditis elegans p38 MAPK Gene plays a key role in protection from mycobacteria

The Caenorhabditis elegans p38 MAPK Gene plays a key role in protection from mycobacteria

Mechanisms of innate immunity inC. elegansepidermis

Conidia of the nematophagous fungus Drechmeria coniospora adhere to but barely infect Acrobeloides buetschilii

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