M3i

@article{Huang2023,

title = {A Toll pathway effector protects Drosophila specifically from distinct toxins secreted by a fungus or a bacterium},

author = {Jianqiong Huang and Yanyan Lou and Jiyong Liu and Philippe Bulet and Chuping Cai and Kaiyu Ma and Renjie Jiao and Jules A Hoffmann and Samuel Liégeois and Zi Lia and Dominique Ferrandon},

editor = {Hugo Bellen, Baylor College of Medicine, Houston, TX},

url = {https://doi.org/10.1073/pnas.2205140120},

doi = {10.1073/pnas.2205140120},

year  = {2023},

date = {2023-03-14},

urldate = {2023-03-14},

journal = {PNAS},

volume = {120},

number = {12},

abstract = {Major immune response pathways control the expression of hundreds of genes that represent potential effectors of the immune response. The Drosophila Toll pathway is required in the host defenses against several Gram-positive bacterial infections as well as against fungal infections. The current paradigm is that peptides secreted in the hemolymph during the systemic immune response are either bona fide antimicrobial peptides or likely ones. The finding of a dual role for one Toll pathway effector in the resilience to both Enterococcus faecalis and Metarhizium robertsii infections underscores an original concept in insect innate immunity. Evolution can select effectors tailored to protect the host from the action of microbial toxins of prokaryotic or eukaryotic origin, independently of antibodies or detoxification pathways.},

keywords = {Baramicin A, Destruxin A, disease tolerance, enterocin O16, ferrandon, hoffmann, M3i, microbial toxins, resilience},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36322050,

title = {The Toll pathway mediates Drosophila resilience to Aspergillus mycotoxins through specific Bomanins},

author = {Rui Xu and Yanyan Lou and Antonin Tidu and Philippe Bulet and Thorsten Heinekamp and Franck Martin and Axel Brakhage and Zi Li and Samuel Liégeois and Dominique Ferrandon},

url = {https://pubmed.ncbi.nlm.nih.gov/36322050/},

doi = {10.15252/embr.202256036},

issn = {1469-3178},

year  = {2022},

date = {2022-11-01},

urldate = {2022-11-01},

journal = {EMBO Rep},

pages = {e56036},

abstract = {Host defense against infections encompasses both resistance, which targets microorganisms for neutralization or elimination, and resilience/disease tolerance, which allows the host to withstand/tolerate pathogens and repair damages. In Drosophila, the Toll signaling pathway is thought to mediate resistance against fungal infections by regulating the secretion of antimicrobial peptides, potentially including Bomanins. We find that Aspergillus fumigatus kills Drosophila Toll pathway mutants without invasion because its dissemination is blocked by melanization, suggesting a role for Toll in host defense distinct from resistance. We report that mutants affecting the Toll pathway or the 55C Bomanin locus are susceptible to the injection of two Aspergillus mycotoxins, restrictocin and verruculogen. The vulnerability of 55C deletion mutants to these mycotoxins is rescued by the overexpression of Bomanins specific to each challenge. Mechanistically, flies in which BomS6 is expressed in the nervous system exhibit an enhanced recovery from the tremors induced by injected verruculogen and display improved survival. Thus, innate immunity also protects the host against the action of microbial toxins through secreted peptides and thereby increases its resilience to infection.},

keywords = {ERIANI, ferrandon, M3i, MARTIN, Unité ARN},

pubstate = {published},

tppubtype = {article}

}

@article{Liégeois2020b,

title = {An atlas for hemocytes in an insect},

author = {Samuel Liégeois and Dominique Ferrandon},

editor = {Elife},

url = {https://elifesciences.org/articles/59113},

doi = {10.7554/eLife.59113},

year  = {2020},

date = {2020-06-30},

journal = {Elife},

abstract = {Single-cell RNA sequencing has revealed distinct subpopulations of hemocytes in fruit fly larvae},

keywords = {Drosophila, ferrandon, Hemocytes, M3i, single-cell},

pubstate = {published},

tppubtype = {article}

}

@article{Franchet2019,

title = {Phosphatidic acid as a limiting host metabolite for the proliferation of the microsporidium Tubulinosema ratisbonensis in Drosophila flies},

author = {Adrien Franchet and Sebastian Niehus and Gaetan Caravello and Dominique Ferrandon},

editor = {Nature Publishing Group},

url = {https://www.nature.com/articles/s41564-018-0344-y},

doi = {10.1038/s41564-018-0344-y},

isbn = {2058-5276},

year  = {2019},

date = {2019-01-28},

journal = {Nature Microbiology},

volume = {4},

number = {4},

pages = {645},

abstract = {A Drosophila melanogaster systemic infection model for the microsporidian Tubulinosema ratisbonensis reveals that the parasite hijacks host phosphatidic acid, which is a limiting precursor for synthesis of parasite membranes and therefore proliferation.},

keywords = {Drosophila, ferrandon, Host-Parasite Interactions, Lipids, M3i, metabolism, microsporidia},

pubstate = {published},

tppubtype = {article}

}

@article{S2018,

title = {Quorum-sensing regulator RhlR but not its autoinducer RhlI enables Pseudomonas to evade opsonization},

author = {Samantha Haller and Adrien Franchet and A Hakkim and J Chen and E Drenkard and S Yu and Steffi Schirmeier and Zi Li and Nelson Martins and FM Ausubel and Samuel Liégeois and Dominique Ferrandon},

url = {http://embor.embopress.org/content/early/2018/03/09/embr.201744880},

doi = {10.15252/embr.201744880},

year  = {2018},

date = {2018-03-09},

journal = {EMBO Reports},

keywords = {Drosophila, ferrandon, M3i, Opsonin Proteins, Phagocytosis, Pseudomonas aeruginosa, Quorum Sensing},

pubstate = {published},

tppubtype = {article}

}

@article{Lee2016,

title = {Enterocyte Purge and Rapid Recovery Is a Resilience Reaction of the Gut Epithelium to Pore-Forming Toxin Attack},

author = {Kwang-Zin Lee and Matthieu Lestradet and Catherine Socha and Stefanie Schirmeier and Antonin Schmitz and Caroline Spenlé and Olivier Lefebvre and Céline Keime and Wennida M. Yamba and Richard Bou Aoun and Samuel Liegeois and Yannick Schwab and Patricia Simon-Assmann and Frédéric Dalle and Dominique Ferrandon},

editor = {L Abate},

url = {http://www.sciencedirect.com/science/article/pii/S193131281630436X},

doi = {10.1016/j.chom.2016.10.010},

issn = {1931-3128},

year  = {2016},

date = {2016-11-23},

urldate = {2016-11-25},

journal = {Cell Host & Microbe},

abstract = {Summary 

Besides digesting nutrients, the gut protects the host against invasion by pathogens. Enterocytes may be subjected to damage by both microbial and host defensive responses, causing their death. Here, we report a rapid epithelial response that alleviates infection stress and protects the enterocytes from the action of microbial virulence factors. Intestinal epithelia exposed to hemolysin, a pore-forming toxin secreted by Serratia marcescens, undergo an evolutionarily conserved process of thinning followed by the recovery of their initial thickness within a few hours. In response to hemolysin attack, Drosophila melanogaster enterocytes extrude most of their apical cytoplasm, including damaged organelles such as mitochondria, yet do not lyse. We identify two secreted peptides, the expression of which requires CyclinJ, that mediate the recovery phase in which enterocytes regain their original shape and volume. Epithelial thinning and recovery constitute a fast and efficient response to intestinal infections, with pore-forming toxins acting as alarm signals.},

keywords = {Epithelium, ferrandon, gut, M3i, resilience},

pubstate = {published},

tppubtype = {article}

}

@article{brunke_mice_2015b,

title = {Of mice, flies--and men? Comparing fungal infection models for large-scale screening efforts},

author = {Sascha Brunke and Jessica Quintin and Lydia Kasper and Ilse D Jacobsen and Martin E Richter and Ekkehard Hiller and Tobias Schwarzmüller and Christophe d'Enfert and Karl Kuchler and Steffen Rupp and Bernhard Hube and Dominique Ferrandon},

url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415897/},

doi = {10.1242/dmm.019901},

issn = {1754-8411},

year  = {2015},

date = {2015-01-01},

journal = {Dis Model Mech},

volume = {8},

number = {5},

pages = {473--486},

abstract = {Studying infectious diseases requires suitable hosts for experimental in vivo infections. Recent years have seen the advent of many alternatives to murine infection models. However, the use of non-mammalian models is still controversial because it is often unclear how well findings from these systems predict virulence potential in humans or other mammals. Here, we compare the commonly used models, fruit fly and mouse (representing invertebrate and mammalian hosts), for their similarities and degree of correlation upon infection with a library of mutants of an important fungal pathogen, the yeast Candida glabrata. Using two indices, for fly survival time and for mouse fungal burden in specific organs, we show a good agreement between the models. We provide a suitable predictive model for estimating the virulence potential of C. glabrata mutants in the mouse from fly survival data. As examples, we found cell wall integrity mutants attenuated in flies, and mutants of a MAP kinase pathway had defective virulence in flies and reduced relative pathogen fitness in mice. In addition, mutants with strongly reduced in vitro growth generally, but not always, had reduced virulence in flies. Overall, we demonstrate that surveying Drosophila survival after infection is a suitable model to predict the outcome of murine infections, especially for severely attenuated C. glabrata mutants. Pre-screening of mutants in an invertebrate Drosophila model can, thus, provide a good estimate of the probability of finding a strain with reduced microbial burden in the mouse host.},

keywords = {Alternative infection models, Candida glabrata, ferrandon, Fungal virulence factors, M3i, Mutant library, Signature-tagged mutagenesis},

pubstate = {published},

tppubtype = {article}

}

@article{amcheslavsky_enteroendocrine_2014b,

title = {Enteroendocrine cells support intestinal stem-cell-mediated homeostasis in Drosophila},

author = {Alla Amcheslavsky and Wei Song and Qi Li and Yingchao Nie and Ivan Bragatto and Dominique Ferrandon and Norbert Perrimon and Tony Y Ip},

doi = {10.1016/j.celrep.2014.08.052},

issn = {2211-1247},

year  = {2014},

date = {2014-10-01},

journal = {Cell Rep},

volume = {9},

number = {1},

pages = {32--39},

abstract = {Intestinal stem cells in the adult Drosophila midgut are regulated by growth factors produced from the surrounding niche cells including enterocytes and visceral muscle. The role of the other major cell type, the secretory enteroendocrine cells, in regulating intestinal stem cells remains unclear. We show here that newly eclosed scute loss-of-function mutant flies are completely devoid of enteroendocrine cells. These enteroendocrine cell-less flies have normal ingestion and fecundity but shorter lifespan. Moreover, in these newly eclosed mutant flies, the diet-stimulated midgut growth that depends on the insulin-like peptide 3 expression in the surrounding muscle is defective. The depletion of Tachykinin-producing enteroendocrine cells or knockdown of Tachykinin leads to a similar although less severe phenotype. These results establish that enteroendocrine cells serve as an important link between diet and visceral muscle expression of an insulin-like growth factor to stimulate intestinal stem cell proliferation and tissue growth.},

keywords = {Animals, Cell Differentiation, Enterocytes, Enteroendocrine Cells, Female, ferrandon, Homeostasis, Intestines, M3i, Male, Stem Cells, Tachykinins},

pubstate = {published},

tppubtype = {article}

}

@article{haller_assessing_2014b,

title = {Assessing Pseudomonas virulence with a nonmammalian host: Drosophila melanogaster},

author = {Samantha Haller and Stefanie Limmer and Dominique Ferrandon},

doi = {10.1007/978-1-4939-0473-0_56},

issn = {1940-6029},

year  = {2014},

date = {2014-01-01},

journal = {Methods Mol. Biol.},

volume = {1149},

pages = {723--740},

abstract = {Drosophila melanogaster flies represent an interesting model to study host-pathogen interactions as: (1) they are cheap and easy to raise rapidly and do not bring up ethical issues, (2) available genetic tools are highly sophisticated, for instance allowing tissue-specific alteration of gene expression, e.g., of immune genes, (3) they have a relatively complex organization, with distinct digestive tract and body cavity in which local or systemic infections, respectively, take place, (4) a medium throughput can be achieved in genetic screens, for instance looking for Pseudomonas aeruginosa mutants with altered virulence. We present here the techniques used to investigate host-pathogen relationships, namely the two major models of infections as well as the relevant parameters used to monitor the infection (survival, bacterial titer, induction of host immune response).},

keywords = {Animal, Animals, Antimicrobial Cationic Peptides, Biological Assay, Colony Count, Disease Models, ferrandon, Hemolymph, Host-Pathogen Interactions, M3i, Mammals, Microbial, Pseudomonas aeruginosa, Pseudomonas Infections, Reverse Transcriptase Polymerase Chain Reaction, Virulence},

pubstate = {published},

tppubtype = {article}

}

@article{lestradet_drosophila_2014b,

title = {Drosophila as a model for intestinal infections},

author = {Matthieu Lestradet and Kwan Zin Lee and Dominique Ferrandon},

doi = {10.1007/978-1-4939-1261-2_2},

issn = {1940-6029 (Electronic) 1064-3745 (Linking)},

year  = {2014},

date = {2014-01-01},

journal = {Methods Mol Biol},

volume = {1197},

pages = {11--40},

abstract = {Drosophila melanogaster is a powerful model to study infections thanks to the power of its genetics and knowledge on its biology accumulated for over a century. While the systemic humoral immune response against invading microbes has been intensively studied in the past two decades, the study of intestinal infections is more recent. Here, we present the methods that are currently in use to probe various aspects of the host-pathogen interactions between Drosophila and ingested microbes, with an emphasis on the study of the midgut epithelium, which constitutes the major interface between the organism and the microbe-rich ingested food.},

keywords = {Animal, Animals, Bacterial Physiological Phenomena, Disease Models, ferrandon, Gastrointestinal Tract, Host-Pathogen Interactions, M3i},

pubstate = {published},

tppubtype = {article}

}

@article{schwarzmuller_systematic_2014b,

title = {Systematic phenotyping of a large-scale Candida glabrata deletion collection reveals novel antifungal tolerance genes},

author = {Tobias Schwarzmüller and Biao Ma and Ekkehard Hiller and Fabian Istel and Michael Tscherner and Sascha Brunke and Lauren Ames and Arnaud Firon and Brian Green and Vitor Cabral and Marina Marcet-Houben and Ilse D Jacobsen and Jessica Quintin and Katja Seider and Ingrid Frohner and Walter Glaser and Helmut Jungwirth and Sophie Bachellier-Bassi and Murielle Chauvel and Ute Zeidler and Dominique Ferrandon and Toni Gabaldón and Bernhard Hube and Christophe d'Enfert and Steffen Rupp and Brendan Cormack and Ken Haynes and Karl Kuchler},

doi = {10.1371/journal.ppat.1004211},

issn = {1553-7374},

year  = {2014},

date = {2014-01-01},

journal = {PLoS Pathog.},

volume = {10},

number = {6},

pages = {e1004211},

abstract = {The opportunistic fungal pathogen Candida glabrata is a frequent cause of candidiasis, causing infections ranging from superficial to life-threatening disseminated disease. The inherent tolerance of C. glabrata to azole drugs makes this pathogen a serious clinical threat. To identify novel genes implicated in antifungal drug tolerance, we have constructed a large-scale C. glabrata deletion library consisting of 619 unique, individually bar-coded mutant strains, each lacking one specific gene, all together representing almost 12% of the genome. Functional analysis of this library in a series of phenotypic and fitness assays identified numerous genes required for growth of C. glabrata under normal or specific stress conditions, as well as a number of novel genes involved in tolerance to clinically important antifungal drugs such as azoles and echinocandins. We identified 38 deletion strains displaying strongly increased susceptibility to caspofungin, 28 of which encoding proteins that have not previously been linked to echinocandin tolerance. Our results demonstrate the potential of the C. glabrata mutant collection as a valuable resource in functional genomics studies of this important fungal pathogen of humans, and to facilitate the identification of putative novel antifungal drug target and virulence genes.},

keywords = {Antifungal Agents, Azoles, Biofilms, Candida glabrata, Candidiasis, Cell Wall, Drug Resistance, Echinocandins, ferrandon, Fungal, Fungal Proteins, Gene Deletion, Gene Knockout Techniques, Gene Library, M3i, Microbial Sensitivity Tests, Osmotic Pressure, Phenotype},

pubstate = {published},

tppubtype = {article}

}

@article{quintin_drosophila_2013b,

title = {The Drosophila Toll pathway controls but does not clear Candida glabrata infections},

author = {Jessica Quintin and Joelle Asmar and Alexey A Matskevich and Marie-Céline Lafarge and Dominique Ferrandon},

doi = {10.4049/jimmunol.1201861},

issn = {1550-6606},

year  = {2013},

date = {2013-03-01},

journal = {J. Immunol.},

volume = {190},

number = {6},

pages = {2818--2827},

abstract = {The pathogenicity of Candida glabrata to patients remains poorly understood for lack of convenient animal models to screen large numbers of mutants for altered virulence. In this study, we explore the minihost model Drosophila melanogaster from the dual perspective of host and pathogen. As in vertebrates, wild-type flies contain C. glabrata systemic infections yet are unable to kill the injected yeasts. As for other fungal infections in Drosophila, the Toll pathway restrains C. glabrata proliferation. Persistent C. glabrata yeasts in wild-type flies do not appear to be able to take shelter in hemocytes from the action of the Toll pathway, the effectors of which remain to be identified. Toll pathway mutant flies succumb to injected C. glabrata. In this immunosuppressed background, cellular defenses provide a residual level of protection. Although both the Gram-negative binding protein 3 pattern recognition receptor and the Persephone protease-dependent detection pathway are required for Toll pathway activation by C. glabrata, only GNBP3, and not psh mutants, are susceptible to the infection. Both Candida albicans and C. glabrata are restrained by the Toll pathway, yet the comparative study of phenoloxidase activation reveals a differential activity of the Toll pathway against these two fungal pathogens. Finally, we establish that the high-osmolarity glycerol pathway and yapsins are required for virulence of C. glabrata in this model. Unexpectedly, yapsins do not appear to be required to counteract the cellular immune response but are needed for the colonization of the wild-type host.},

keywords = {Adaptor Proteins, Animal, Animals, Antigens, Candida glabrata, Candidiasis, Cells, Cultured, Differentiation, Disease Models, ferrandon, Immunologic, M3i, Phagocytosis, Receptors, Signal Transducing, Signal Transduction, Toll-Like Receptors, Virulence},

pubstate = {published},

tppubtype = {article}

}

@article{ferrandon_complementary_2013b,

title = {The complementary facets of epithelial host defenses in the genetic model organism Drosophila melanogaster: from resistance to resilience},

author = {Dominique Ferrandon},

doi = {10.1016/j.coi.2012.11.008},

issn = {1879-0372},

year  = {2013},

date = {2013-02-01},

journal = {Curr. Opin. Immunol.},

volume = {25},

number = {1},

pages = {59--70},

abstract = {Significant advances have been made in our understanding of the host defense against microbial infections taking place at frontier epithelia of Drosophila flies. Immune deficiency (IMD), the major NF-κB immune response pathway induced in these epithelia, displays remarkable adaptations in its activation and regulation in the respiratory and digestive tract. The host defense against ingested pathogens is not limited to resistance, that is, the immune response. It also involves resilience, the capacity of the host to endure and repair damages inflicted by pathogens or the host's own immune response. For instance, enterocytes damaged by pathogens, the microbiota of aging flies, or host-derived reactive oxygen species (ROS), are replaced under the control of multiple pathways by the compensatory proliferation of intestinal stem cells (ISCs).},

keywords = {Adult Stem Cells, aging, Animal, Animals, Cell Proliferation, Disease Models, Enterocytes, ferrandon, Humans, Immunity, Intestinal Mucosa, M3i, Metagenome, Stem Cell Niche, Wound Healing},

pubstate = {published},

tppubtype = {article}

}

@article{ayyaz_negative_2013b,

title = {A negative role for MyD88 in the resistance to starvation as revealed in an intestinal infection of Drosophila melanogaster with the Gram-positive bacterium Staphylococcus xylosus},

author = {Arshad Ayyaz and Philippe Giammarinaro and Samuel Liégeois and Matthieu Lestradet and Dominique Ferrandon},

doi = {10.1016/j.imbio.2012.07.027},

issn = {1878-3279},

year  = {2013},

date = {2013-01-01},

journal = {Immunobiology},

volume = {218},

number = {4},

pages = {635--644},

abstract = {Drosophila melanogaster is a useful model to investigate mucosal immunity. The immune response to intestinal infections is mediated partly by the Immune deficiency (IMD) pathway, which only gets activated by a type of peptidoglycan lacking in several medically important Gram-positive bacterial species such as Staphylococcus. Thus, the intestinal host defense against such bacterial strains remains poorly known. Here, we have used Staphylococcus xylosus to develop a model of intestinal infections by Gram-positive bacteria. S. xylosus behaves as an opportunistic pathogen in a septic injury model, being able to kill only flies immunodeficient either for the Toll pathway or the cellular response. When ingested, it is controlled by IMD-independent host intestinal defenses, yet flies eventually die. Having excluded an overreaction of the immune response and the action of toxins, we find that flies actually succumb to starvation, likely as a result of a competition for sucrose between the bacteria and the flies. Fat stores of wild-type flies are severely reduced within a day, a period when sucrose is not yet exhausted in the feeding solution. Interestingly, the Toll pathway mutant MyD88 is more resistant to the ingestion of S. xylosus and to starvation than wild-type flies. MyD88 flies do not rapidly deplete their fat stores when starved, in contrast to wild-type flies. Thus, we have uncovered a novel function of MyD88 in the regulation of metabolism that appears to be independent of its known roles in immunity and development.},

keywords = {Adaptor Proteins, Animal, Animals, Antigens, Differentiation, Disease Models, ferrandon, Immunity, Immunologic, Innate, Intestinal Diseases, M3i, Mucosal, Mutation, Receptors, Signal Transducing, Staphylococcal Infections, Staphylococcus, Starvation, Toll-Like Receptors},

pubstate = {published},

tppubtype = {article}

}

@article{ezekowitz_lawrences_2012,

title = {Lawrence's book review unfair to Hoffmann},

author = {Alan R B Ezekowitz and Jean-Luc Dimarcq and Fotis Kafatos and Elena A Levashina and Dominique Ferrandon and Charles Hetru and Jean-Luc Imler and Jean-Marc Reichhart},

doi = {10.1016/j.cub.2012.05.015},

issn = {1879-0445},

year  = {2012},

date = {2012-06-01},

journal = {Curr. Biol.},

volume = {22},

number = {12},

pages = {R482},

keywords = {Book Reviews as Topic, Ethics, ferrandon, imler, M3i, Professional, reichhart},

pubstate = {published},

tppubtype = {article}

}

@article{niehus_fly_2012b,

title = {Fly culture collapse disorder: detection, prophylaxis and eradication of the microsporidian parasite Tubulinosema ratisbonensis infecting Drosophila melanogaster},

author = {Sebastian Niehus and Philippe Giammarinaro and Samuel Liégeois and Jessica Quintin and Dominique Ferrandon},

doi = {10.4161/fly.20896},

issn = {1933-6942},

year  = {2012},

date = {2012-01-01},

journal = {Fly (Austin)},

volume = {6},

number = {3},

pages = {193--204},

abstract = {Drosophila melanogaster is a robust model to investigate many biological problems. It is however prone to some infections, which may endanger fly stocks if left unchecked for. One such infection is caused by an obligate fungal intracellular parasite, Tubulinosema ratisbonensis, which can be found in laboratory stocks. Here, we identify and briefly characterize a T. ratisbonensis strain that was infesting our Drosophila cultures and that required intensive measures to contain and eradicate the infection. We describe the phenotypes of infested stocks. We also report PCR-based techniques that allow the detection of infested stocks with a high sensitivity. We have developed a high-throughput qPCR assay that allows the efficient parallel screening of a large number of potentially-infested stocks. We also have investigated several prophylactic measures to prevent the further contamination of stocks, namely UV-exposure, ethanol treatment, bleaching, and desiccation. Bleaching was found to kill all spores. Other treatments were less effective but were found to be sufficient to prevent further contamination of noninfested stocks. Two treatments were efficacious in curing infested stocks (1) bleaching of eggs and subsequent raising of the larvae in clean vials; (2) fumagillin treatment. These cures only work on stocks that have not become too weak to withstand the procedures.},

keywords = {Animals, Apansporoblastina, Apansporoblastina/*genetics/physiology, Base Sequence, cure, Disinfection, Disinfection/methods, DNA, DNA Primers, Drosophila melanogaster/*microbiology, ferrandon, fumagillin, Fungal, Fungal/chemistry, M3i, microsporidia, obligate intracellular parasitism, PCR detection, Phylogeny, Polymerase Chain Reaction, Polymerase Chain Reaction/methods, prophylaxis, Ribosomal, Ribosomal/chemistry, Sequence Alignment, Tubulinosema ratisbonensis},

pubstate = {published},

tppubtype = {article}

}