The Toll and Imd pathways are the major regulators of the immune response in Drosophila
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Open Access
- 3 June 2002
- journal article
- research article
- Published by Springer Nature in The EMBO Journal
- Vol. 21 (11) , 2568-2579
- https://doi.org/10.1093/emboj/21.11.2568
Abstract
Microarray studies have shown recently that microbial infection leads to extensive changes in the Drosophila gene expression programme. However, little is known about the control of most of the fly immune‐responsive genes, except for the antimicrobial peptide (AMP)‐encoding genes, which are regulated by the Toll and Imd pathways. Here, we used oligonucleotide microarrays to monitor the effect of mutations affecting the Toll and Imd pathways on the expression programme induced by septic injury in Drosophila adults. We found that the Toll and Imd cascades control the majority of the genes regulated by microbial infection in addition to AMP genes and are involved in nearly all known Drosophila innate immune reactions. However, we identified some genes controlled by septic injury that are not affected in double mutant flies where both Toll and Imd pathways are defective, suggesting that other unidentified signalling cascades are activated by infection. Interestingly, we observed that some Drosophila immune‐responsive genes are located in gene clusters, which often are transcriptionally co‐regulated.Keywords
This publication has 33 references indexed in Scilit:
- Requirement for a Peptidoglycan Recognition Protein (PGRP) in Relish Activation and Antibacterial Immune Responses in DrosophilaScience, 2002
- Functional genomic analysis of phagocytosis and identification of a Drosophila receptor for E. coliNature, 2002
- The Drosophila immune response against Gram-negative bacteria is mediated by a peptidoglycan recognition proteinNature, 2002
- How Drosophila combats microbial infection: a model to study innate immunity and host–pathogen interactionsCurrent Opinion in Microbiology, 2002
- Drosophila Toll is activated by Gram-positive bacteria through a circulating peptidoglycan recognition proteinNature, 2001
- The Plasticity of Dendritic Cell Responses to Pathogens and Their ComponentsScience, 2001
- A Drosophila MAPKKK, D-MEKK1, mediates stress responses through activation of p38 MAPKThe EMBO Journal, 2001
- Expression and Evolution of the Drosophila Attacin/Diptericin Gene FamilyBiochemical and Biophysical Research Communications, 2000
- Relish, a Central Factor in the Control of Humoral but Not Cellular Immunity in DrosophilaPublished by Elsevier ,1999
- In Vivo Regulation of the IκB Homologue cactus during the Immune Response of DrosophilaJournal of Biological Chemistry, 1998