FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Reference Report
Open Close
Reference
Citation
Gross, I., Georgel, P., Kappler, C., Reichhart, J.M., Hoffmann, J.A. (1996). Drosophila immunity: a comparative analysis of the Rel proteins dorsal and Dif in the induction of the genes encoding diptericin and cecropin.  Nucleic Acids Res. 24(7): 1238--1245.
FlyBase ID
FBrf0087267
Publication Type
Research paper
Abstract
In Drosophila, bacterial challenge induces the rapid transcription of several genes encoding potent antibacterial peptides. The upstream sequences of the diptericin and cecropin Al genes, which have been investigated in detail, contain two, respectively one sequence element homologous to the binding site of the mammalian nuclear factor kappaB. These elements have been shown to be mandatory for immune-induced transcription of both genes. Functional studies have shown that these kappaB-related elements can be the target for the Drosophila Rel proteins dorsal and Dif. Here we present a comparative analysis of the transactivating capacities of these proteins on reporter genes fused to either the diptericin or the cecropin kappaB-related motifs. We conclude from our results: (i) the kappaB motifs of the diptericin and cecropin genes are not functionally equivalent; (ii) the dorsal and Dif proteins have distinct DNA-binding characteristics; (iii) dorsal and Dif can heterodimerize in vitro; (iv) mutants containing no copies of dorsal and a single copy of Dif retain their full capacity to express the diptericin and cecropin genes in response to challenge.
PubMed ID
PubMed Central ID
PMC145794 (PMC) (EuropePMC)
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Nucleic Acids Res.
    Title
    Nucleic Acids Research
    Publication Year
    1974-
    ISBN/ISSN
    0305-1048
    Data From Reference
    Aberrations (2)
    Alleles (2)
    Genes (5)
    Cell Lines (1)