ArticleProceedings of the National Academy of Sciences of the United States of America2006
Anthrax lethal factor and edema factor act on conserved targets in Drosophila.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
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- Silkworm model forVirulence · 2021Article
- Distinct roles of Bendless in regulating FSC niche competition and daughter cell differentiation.Development (Cambridge, England) · 2021Article
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- Anthrax toxin component, Protective Antigen, protects insects from bacterial infections.PLoS pathogens · 2020Article
- A Drosophila Model for Clostridium difficile Toxin CDT Reveals Interactions with Multiple Effector Pathways.iScience · 2020Article
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- Anthrax edema toxin disrupts distinct steps in Rab11-dependent junctional transport.PLoS pathogens · 2017Article
- RAB11-mediated trafficking in host-pathogen interactions.Nature reviews. Microbiology · 2014Review
- Toxin inhibition of antimicrobial factors induced by Bacillus anthracis peptidoglycan in human blood.Infection and immunity · 2013Article
- The Hedgehog signal transduction network.Science signaling · 2012Review
- Aeromonas salmonicida-secreted protein AopP is a potent inducer of apoptosis in a mammalian and a Drosophila model.Cellular microbiology · 2012Article
- Review
- New insights into the biological effects of anthrax toxins: linking cellular to organismal responses.Microbes and infection · 2012Review
- The Drosophila melanogaster host model.Journal of oral microbiology · 2012Article
- Deconstructing host-pathogen interactions in Drosophila.Disease models & mechanisms · 2012Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Many bacterial toxins act on conserved components of essential host-signaling pathways. One consequence of this conservation is that genetic model organisms such as Drosophila melanogaster can be used for analyzing the mechanism of toxin action. In this study, we characterize the activities of two anthrax virulence factors, lethal factor (LF) and edema factor, in transgenic Drosophila. LF is a zinc metalloprotease that cleaves and inactivates most human mitogen-activated protein kinase (MAPK) kinases (MAPKKs). We found that LF similarly cleaves the Drosophila MAPK kinases Hemipterous (Hep) and Licorne in vitro. Consistent with these observations, expression of LF in Drosophila inhibited the Hep/c-Jun N-terminal kinase pathway during embryonic dorsal closure and the related process of adult thoracic closure. Epistasis experiments confirmed that LF acts at the level of Hep. We also found that LF inhibits Ras/MAPK signaling during wing development and that LF acts upstream of MAPK and downstream of Raf, consistent with LF acting at the level of Dsor. In addition, we found that edema factor, a potent adenylate cyclase, inhibits the hh pathway during wing development, consistent with the known role of cAMP-dependent PKA in suppressing the Hedgehog response. These results demonstrate that anthrax toxins function in Drosophila as they do in mammalian cells and open the way to using Drosophila as a multicellular host system for studying the in vivo function of diverse toxins and virulence factors.
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