ArticleJournal of innate immunity2017
Thioester-Containing Protein-4 Regulates the Drosophila Immune Signaling and Function against the Pathogen Photorhabdus.
Article in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 43 citations in OpenAlex.
- Knockouts of Sulfur Metabolism Genes Induce Chronic Inflammation and Immune Dysregulation inAntioxidants (Basel, Switzerland) · 2026Article
- α2-macroglobulin function of thioester-containing proteins guardsProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Immune Reactions of Vector Insects to Parasites and Pathogens.Microorganisms · 2024Review
- Mycobacterium abscessus Opsonization Allows an Escape from the Defensin Bactericidal Action inMicrobiology spectrum · 2023Article
- Growth deregulation and interaction with host hemocytes contribute to tumor progression in a Drosophila brain tumor model.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Interactions between innate immunity and insulin signaling affect resistance to infection in insects.Frontiers in immunology · 2023Review
- Pharmacological or genetic inhibition of hypoxia signaling attenuates oncogenic RAS-induced cancer phenotypes.Disease models & mechanisms · 2022Article
- Molecular characterization of thioester-containing proteins inFrontiers in immunology · 2022Article
- Haemocyte-mediated immunity in insects: Cells, processes and associated components in the fight against pathogens and parasites.Immunology · 2021Review
- Review
- Single-cell RNA sequencing identifies novel cell types in Drosophila blood.Journal of genetics and genomics = Yi chuan xue bao · 2020Article
- Biomphalaria glabrata immunity: Post-genome advances.Developmental and comparative immunology · 2020Review
- Thioester-containing Proteins in theInsects · 2020Review
- Participation of the Serine Protease Jonah66Ci in theInfection and immunity · 2019Article
- Intestinal lipid droplets as novel mediators of host-pathogen interaction inBiology open · 2019Article
- Tackling the Pros and Cons of Inflammation.Journal of innate immunity · 2019Article
- Quorum-sensing regulator RhlR but not its autoinducer RhlI enablesEMBO reports · 2018Article
- Thioester-Containing Proteins 2 and 4 Affect the Metabolic Activity and Inflammation Response in Drosophila.Infection and immunity · 2018Article
- Rapid seasonal evolution in innate immunity of wildProceedings. Biological sciences · 2018Article
- Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite important progress in identifying the molecules that participate in the immune response of Drosophila melanogaster to microbial infections, the involvement of thioester-containing proteins (TEPs) in the antibacterial immunity of the fly is not fully clarified. Previous studies mostly focused on identifying the function of TEP2, TEP3 and TEP6 molecules in the D. melanogaster immune system. Here, we investigated the role of TEP4 in the regulation and function of D. melanogaster host defense against 2 virulent pathogens from the genus Photorhabdus, i.e. the insect pathogenic bacterium Photorhabdus luminescens and the emerging human pathogen P. asymbiotica. We demonstrate that Tep4 is strongly upregulated in adult flies following the injection of Photorhabdus bacteria. We also show that Tep4 loss-of-function mutants are resistant to P. luminescens but not to P. asymbiotica infection. In addition, we find that inactivation of Tep4 results in the upregulation of the Toll and Imd immune pathways, and the downregulation of the Jak/Stat and Jnk pathways upon Photorhabdus infection. We document that loss of Tep4 promotes melanization and phenoloxidase activity in the mutant flies infected with Photorhabdus. Together, these findings generate novel insights into the immune role of TEP4 as a regulator and effector of the D. melanogaster antibacterial immune response.
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