Escherichia coli Infection of Drosophila

Tracy, Charles; Krämer, Helmut

doi:10.21769/bioprotoc.2256

Cited by 5 publications

(3 citation statements)

References 5 publications

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“…Wildtype Oregon-R Drosophila flies were treated with sucrose solutions containing various concentrations of S. cerevisiae ( Fig. 2a and Additional file 2), and compared to the pathogenicity of known entomopathogenic Gram-positive Bacillus cereus and Micrococcus luteus, as well as Gram-negative Escherichia coli and Serratia liquefaciens bacteria [7,[20][21][22] (Figs. 2b-e, respectively).…”

Section: Susceptibility Of Drosophila Melanogaster To Saccharomyces Cmentioning

confidence: 99%

Identification of glucocorticoid receptor in Drosophila melanogaster

et al. 2020

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Background: Vertebrate glucocorticoid receptor (GR) is an evolutionary-conserved cortisol-regulated nuclear receptor that controls key metabolic and developmental pathways. Upon binding to cortisol, GR acts as an immunosuppressive transcription factor. Drosophila melanogaster, a model organism to study innate immunity, can also be immunosuppressed by glucocorticoids. However, while the genome of fruit fly harbors 18 nuclear receptor genes, the functional homolog of vertebrate GR has not been identified. Results: In this study, we demonstrated that while D. melanogaster is susceptible to Saccharomyces cerevisiae oral infection, the oral exposure to cortisol analogs, cortisone acetate or estrogen, increases fly sensitivity to yeast challenge. To understand the mechanism of this steroid-induced immunosuppression, we identified the closest genetic GR homolog as D. melanogaster Estrogen Related Receptor (ERR) gene. We discovered that Drosophila ERR is necessary for cortisone acetate-and estrogen-mediated increase in sensitivity to fungal infection: while ERR mutant flies are as sensitive to the fungal challenge as the wildtype flies, the yeast-sensitivity of ERR mutants is not increased by these steroids. Interestingly, the fungal cortisone analog, ergosterol, did not increase the susceptibility of Drosophila to yeast infection. The immunosuppressive effect of steroids on the sensitivity of flies to fungi is evolutionary conserved in insects, as we show that estrogen significantly increases the yeast-sensitivity of Culex quinquefasciatus mosquitoes, whose genome contains a close ortholog of the fly ERR gene. Conclusions: This study identifies a D. melanogaster gene that structurally resembles vertebrate GR and is functionally necessary for the steroid-mediated immunosuppression to fungal infections.

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Section: Susceptibility Of Drosophila Melanogaster To Saccharomyces Cmentioning

confidence: 99%

Identification of glucocorticoid receptor in Drosophila melanogaster

et al. 2020

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“…Infection experiments were performed as described previously 30,31,78 . In brief, virgins (4‐5 days old) were injected with 80 nL PBS containing a mean of 1600 heated‐killed E. coli (DH5α, GFP, OD600 = 0.1) using a pico‐injector (model PLI‐188; Nikon).…”

Section: Methodsmentioning

confidence: 99%

Hypersensitivity of Vps33B mutant flies to non‐pathogenic infections is dictated by aberrant activation of p38b MAP kinase

Zhang

Tracy

Pasare

et al. 2020

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Loss of the arthrogryposis‐renal dysfunction‐cholestasis (ARC) syndrome‐linked Vps33B protein results in exaggerated inflammatory responses upon activation of receptors of the innate immune system in both vertebrates and flies. However, little is known about the signaling elements downstream of these receptors that are critical for the hypersensitivity of Vps33B mutants. Here, we show that p38b MAP kinase contributes to the enhanced inflammatory responses in flies lacking Vps33B. Loss of p38b mitogen‐activated protein kinase (MAPK) reduces enhanced inflammatory responses and prolongs the survival of infected Vps33B deficient flies. The function of p38 MAPK is not limited to its proinflammatory effects downstream of the PGRP‐LC receptor as p38 also modulates endosomal trafficking of PGRP‐LC and phagocytosis of bacteria. Expression of constitutively active p38b MAPK, but not dominant negative p38b MAPK enhances accumulation of endocytosed PGRP‐LC receptors or phagocytosed bacteria within cells. Moreover, p38 MAPK is required for induction of macropinocytosis, an alternate pathway for the downregulation of immune receptors. Together, our data indicate that p38 MAPK activates multiple pathways that can contribute to the dysregulation of innate immune signaling in ARC syndrome.

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“…We therefore elected to associate Dmel flies with a strain of Lactobacillus brevis, or with one of Acetobacter pomorum, both of which had been isolated from a laboratory population of Dmel and are frequently used for microbiota studies (19,20). In order to test whether any generic bacterium could restore repellency in axenic Dmel, we also associated Dmel flies with a strain of Escherichia coli previously shown as nonpathogenic to flies (21). Dmel inoculation with L. brevis made Dmel repellent to Ds (p < 0.01) while association with A. pomorum and E. coli did not (Fig.…”

Section: Bacterial Symbionts Of Dmel Are Involved In Repellency and Ds Avoidance Lossmentioning

confidence: 99%

Microbiota-Mediated Competition BetweenDrosophilaSpecies

Rombaut¹,

Gallet²,

Qitout³

et al. 2020

Preprint

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Species that share the same ecological niche often avoid costly competition with contextdependent behaviors. This is the case of the invasive insect pest Drosophila suzukii that can develop in ripe fruit where it encounters Drosophila melanogaster. Previous research showed D. suzukii prevents costly larval competition by not ovipositing in substrates with D. melanogaster eggs. We discovered D. suzukii females respond to cues produced by bacteria in the gut microbiome of D. melanogaster. This behavior of D. suzukii varied over time and among populations, revealing subtle condition-dependence. In particular, D. suzukii females that bore D. melanogaster bacteria stopped avoiding sites with D. melanogaster cues. The adaptive significance of the behavior was investigated by reproducing experimentally in-fruit larval competition. D. suzukii larvae only suffered from competition with D. melanogaster if the competitor was associated to its microbiota, suggesting D. suzukii has evolved a solution to avoid offspring develops in challenging environments. We argue that D. suzukii’s competition avoidance behavior has features enabling the design of an evolution-proof repellent to protect crops.

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Escherichia coli Infection of Drosophila

Cited by 5 publications

References 5 publications

Identification of glucocorticoid receptor in Drosophila melanogaster

Identification of glucocorticoid receptor in Drosophila melanogaster

Hypersensitivity of Vps33B mutant flies to non‐pathogenic infections is dictated by aberrant activation of p38b MAP kinase

Microbiota-Mediated Competition BetweenDrosophilaSpecies

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