Insect immunity: developmental and inducible activity of the Drosophila diptericin promoter.

Abstract

Diptericins are 9 kDa inducible antibacterial peptides initially isolated from immune haemolymph of Phormia (Diptera). Following the isolation of a Drosophila cDNA encoding a diptericin homologue, we have now cloned a genomic fragment containing the Drosophila diptericin gene. To dissect the regulation of this gene, we have transformed flies with a fusion gene in which the reporter beta‐galactosidase gene is under the control of 2.2 kb upstream sequences of the diptericin gene. We show that such a fusion gene is inducible by injection of live bacteria or complete Freund's adjuvant and respects the tissue specific expression pattern of the resident diptericin gene. Our analysis reveals at least four distinct phases in the regulation of this gene: young larvae, late third instar larvae, pupae and adults. This complexity may be related to the presence in the upstream sequences of multiple copies of response elements previously characterized in genes encoding acute phase response proteins in mammals (e.g. NK‐kappa B, NF‐kappa B related, NF‐IL6 response elements).

The humoral antibacterial response of Drosophila

“…Studies performed on the expression profiles of the genes encoding cecropins [19,20,23], diptericin [21], defensin [25] and drosocin [24] in bacteria-challenged Drosophila yielded results similar to those obtained in other species of the recent insect orders (namely in Hvalophora cecropia (reviewed in [15]), Munduca sexta [26], Sarcophuga peregrina [ 11,27-291, Phormia terranovae [30]). The genes are rapidly transcribed following challenge (1 to 2 h), the transcription rate increases over a period varying between 6 and 24 h, depending on the gene, and thereafter either stops or levels off.…”

Nitric oxide contributes to induction of innate immune responses to gram-negative bacteria inDrosophila

“…Therefore, we conclude that NOS activity is required for Dipt expression after natural infection with gram-negative bacteria, and that NO is sufficient to activate Dipt expression in the absence of infection. Both infection and SNAP treatment resulted in an initial mosaic pattern of GFP in the fat body (data not shown; Reichhart et al 1992). Thus, exogenously provided NO not only activates the Imd pathway in the absence of infection, it also recapitulates this spatial feature of Dipt expression.…”

“…The spz rm7 , domino, and imd mutant strains used have been described elsewhere (Lemaitre et al 1995a(Lemaitre et al , 1996Braun et al 1998;Georgel et al 2001). The reporter strains Dipt-lacZ, Drs-GFP, and Drs-lacZ have been described in Reichhart et al (1992), Ferrandon et al (1998), andManfruelli et al (1999), respectively. Dipt-GFP flies were a gift of Bruno Lemaitre.…”

How Drosophila combats microbial infection: a model to study innate immunity and host–pathogen interactions

“…size of the fat body cells increases dramatically by polyploidization and their immune competence increases under the control of ecdysone [23,24]. In the early adult stage, the larval fat body desegregates and is replaced by a new adult fat body with slightly different immune properties.…”