The Rel Protein DIF Mediates the Antifungal but Not the Antibacterial Host Defense in Drosophila

• Published in: Immunity (Cambridge, Mass.) Vol. 12; no. 5; pp. 569 - 580
• Main Authors: Rutschmann, Sophie, Jung, Alain C, Hetru, Charles, Reichhart, Jean-Marc, Hoffmann, Jules A, Ferrandon, Dominique
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2000
• Subjects: Animals; Antigens, Bacterial - immunology; Antigens, Fungal - immunology; DNA-Binding Proteins - immunology; Drosomycin gene; Drosophila; Drosophila - immunology; Drosophila - microbiology; Drosophila Proteins; Immunity, Innate; NF-^KB-like factor; NF-B-like factor; Transcription Factors
• ISSN: 1074-7613; 1097-4180
• DOI: 10.1016/S1074-7613(00)80208-3

We have isolated two Drosophila lines that carry point mutations in the gene coding for the NF-κB-like factor DIF. Like mutants of the Toll pathway, Dif mutant flies are susceptible to fungal but not to bacterial infections. Genetic epistasis experiments demonstrate that Dif mediates the Toll-dependent control of the inducibility of the antifungal peptide gene Drosomycin. Strikingly, DIF alone is required for the antifungal response in adults, but is redundant in larvae with Dorsal, another Rel family member. In Drosophila, Dif appears to be dedicated to the antifungal defense elicited by fungi and gram-positive bacteria. We discuss in this light the possibility that NF-κB1/p50 might be required more specifically in the innate immune response against gram-positive bacteria in mammals.