38 research outputs found

    Lack of an Antibacterial Response Defect in Drosophila Toll-9 Mutant

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    Toll and Toll-like receptors represent families of receptors involved in mediating innate immunity response in insects and mammals. Although Drosophila proteome contains multiple Toll paralogs, Toll-1 is, so far, the only receptor to which an immune role has been attributed. In contrast, every single mammalian TLR is a key membrane receptor upstream of the vertebrate immune signaling cascades. The prevailing view is that TLR-mediated immunity is ancient. Structural analysis reveals that Drosophila Toll-9 is the most closely related to vertebrate TLRs and utilizes similar signaling components as Toll-1. This suggests that Toll-9 could be an ancestor of TLR-like receptors and could have immune function. Consistently, it has been reported that over-expression of Toll-9 in immune tissues is sufficient to induce the expression of some antimicrobial peptides in flies. These results have led to the idea that Toll-9 could be a constitutively active receptor that maintain significant levels of antimicrobial molecules and therefore provide constant basal protection against micro-organisms. To test theses hypotheses, we generated and analyzed phenotypes associated with a complete loss-of-function allele of Toll-9. Our results suggest that Toll-9 is neither required to maintain a basal anti-microbial response nor to mount an efficient immune response to bacterial infection

    RNA-sequencing elucidates the regulation of behavioural transitions associated with mating in honey bee queens

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    This study was funded by a BBSRC ISIS grant BB/J019453/1, a Royal Holloway Research Strategy Fund Grant, and a Leverhulme Grant F/07537/AK to MJFB. BPO was supported by Australian Research Council Discovery grants DP150100151 and DP120101915. FM was supported by a Marie Curie International Incoming Fellowship FP7-PEOPLE-2013-IIF-625487 to MJFB. We would like to thank Dave Galbraight (Penn State) and Alberto Paccanaro (RHUL) for support with analysis of RNAseq data and four anonymous reviewers for providing thoughtful insights that helped to improve the manuscript.Peer reviewedPublisher PD

    Serpent regulates Drosophila immunity genes in the larval fat body through an essential GATA motif.

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    Insects possess a powerful immune system, which in response to infection leads to a vast production of different antimicrobial peptides. The regulatory regions of many immunity genes contain a GATA motif in proximity to a kappaB motif. Upon infection, Rel proteins enter the nucleus and activate transcription of the immunity genes. High levels of Rel protein-mediated Cecropin A1 expression previously have been shown to require the GATA site along with the kappaB site. We provide evidence demonstrating that the GATA motif is needed for expression of the Cecropin A1 gene in larval fat body, but is dispensable in adult fat body. A nuclear DNA-binding activity interacts with the Cecropin A1 GATA motif with the same properties as the Drosophila GATA factor Serpent. The GATA-binding activity is recognized by Serpent-specific antibodies, demonstrating their identity. We show that Serpent is nuclear in larval fat body cells and haemocytes both before and after infection. After overexpression, Serpent increases Cecropin A1 transcription in a GATA-dependent manner. We propose that Serpent plays a key role in tissue-specific expression of immunity genes, by priming them for inducible activation by Rel proteins in response to infection
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