Treatment of l(2)mbn Drosophila tumorous blood cells with the steroid hormone ecdysone amplifies the inducibility of antimicrobial peptide gene expression

Dimarcq, Jean‐Luc; Imler, Jean‐Luc; Lanot, R; Ezekowitz, R. A. B.; Hoffmann, Jules A.; Janeway, Charles A.; Lagueux, Marie

doi:10.1016/s0965-1748(97)00072-6

Cited by 123 publications

(102 citation statements)

References 39 publications

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“…Ecdysone treatment causes significant changes in the S2* cells, including altered morphology and adherence, cell cycle arrest, and, most importantly, a greater level of LPS-induced antimicrobial peptide gene expression (data not shown and Ref. 45). Also, in our experiments we used printed cDNA arrays that include only ϳ40% of the predicted genes in the fly, whereas Boutros et al used oligo-based arrays that include features for all ϳ14,000 predicted genes (24).…”

Section: Discussionmentioning

confidence: 98%

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Silverman

Zhou²,

Erlich

et al. 2003

Journal of Biological Chemistry

239

230

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Section: Discussionmentioning

confidence: 98%

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Silverman

Zhou²,

Erlich

et al. 2003

Journal of Biological Chemistry

239

230

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“…AF247768). RT-PCR was performed as described (22), and the PCR bands were sequenced to ensure that they correspond to the expected cDNAs.…”

Section: Methodsmentioning

confidence: 99%

“…LPS has been reported to induce the expression of the genes encoding the antimicrobial peptides in the macrophage-like Schneider and l(2)mbn cell lines (see ref. 22 for references), indicating that these cells express functional LPS receptors. We therefore examined expression of Toll-related genes in these cell lines.…”

Section: Differential Expression Of Toll-related Molecules In Drosophmentioning

confidence: 99%

Toll-related receptors and the control of antimicrobial peptide expression inDrosophila

Tauszig

Jouanguy²,

Hoffmann³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

350

300

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Insects defend themselves against infectious microorganisms by synthesizing potent antimicrobial peptides. Drosophila has appeared in recent years as a favorable model to study this innate host defense. A genetic analysis of the regulation of the antifungal peptide drosomycin has demonstrated a key role for the transmembrane receptor Toll, which prompted the search for mammalian homologs. Two of these, Toll-like receptor (TLR)2 and TLR4, recently were shown to play a critical role in innate immunity against bacteria. Here we describe six additional Toll-related genes (Toll-3 to Toll-8) in Drosophila in addition to 18-wheeler. Two of these genes, Toll-3 and Toll-4, are expressed at a low level. Toll-6, -7, and -8, on the other hand, are expressed at high levels during embryogenesis and molting, suggesting that, like Toll and 18w, they perform developmental functions. Finally, Toll-5 is expressed only in larvae and adults. By using chimeric constructs, we have tested the capacity of the signaling Toll͞IL-1R homology domains of these receptors to activate antimicrobial peptide promoters and found that only Toll and Toll-5 can activate the drosomycin promoter in transfected cells, thus demonstrating specificity at the level of the Toll͞IL-1R homology domain. In contrast, none of these constructs activated antibacterial peptide promoters, suggesting that Toll-related receptors are not involved in the regulation of antibacterial peptide expression. This result was independently confirmed by the demonstration that a dominant-negative version of the kinase Pelle can block induction of drosomycin by the cytokine Spaetzle, but does not affect induction of the antibacterial peptide attacin by lipopolysaccharide.

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“…These cells are known to be immune-responsive and are believed to be derived from phagocytes (Ramet et al 2002). We first pretreated the cells with ecdysone, which enhances the innate immune response (Dimarcq et al 1997). Then, 1 d after ecdysone treatment, we exposed the cells to a commercial LPS preparation; such preparations contain Gram-negative bacterial peptidoglycan that induces the Imd pathway (Leulier et al 2003).…”

Section: An Lps Preparation Induces Transient and Sustained Transcripmentioning

confidence: 99%

Targeting of TAK1 by the NF-κB protein Relish regulates the JNK-mediated immune response in Drosophila

Park¹,

Brady²,

Ruocco³

et al. 2004

Genes Dev.

170

157

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The molecular circuitry underlying innate immunity is constructed of multiple, evolutionarily conserved signaling modules with distinct regulatory targets. The MAP kinases and the IKK-NF-B molecules play important roles in the initiation of immune effector responses. We have found that the Drosophila NF-B protein Relish plays a crucial role in limiting the duration of JNK activation and output in response to Gram-negative infections. Relish activation is linked to proteasomal degradation of TAK1, the upstream MAP kinase kinase kinase required for JNK activation. Degradation of TAK1 leads to a rapid termination of JNK signaling, resulting in a transient JNK-dependent response that precedes the sustained induction of Relish-dependent innate immune loci. Because the IKK-NF-B module also negatively regulates JNK activation in mammals, thereby controlling inflammation-induced apoptosis, the regulatory cross-talk between the JNK and NF-B pathways appears to be broadly conserved.

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Treatment of l(2)mbn Drosophila tumorous blood cells with the steroid hormone ecdysone amplifies the inducibility of antimicrobial peptide gene expression

Cited by 123 publications

References 39 publications

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Toll-related receptors and the control of antimicrobial peptide expression inDrosophila

Targeting of TAK1 by the NF-κB protein Relish regulates the JNK-mediated immune response in Drosophila

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