title: Damaged DNA binding protein 1 in Drosophila defense reactions.
abstract: We have focused attention on functions of Drosophila damaged DNA binding protein 1 (D-DDB1) in Drosophila hematopoiesis and previously reported that its whole body dsRNA over-expression using a GAL4-UAS targeted expression system results in melanotic tumors and complete lethality. Since the lesions appear to arise as a normal and heritable response to abnormal development, forming groups of cells that are recognized by the immune system and encapsulated in melanized cuticle, D-DDB1 appears to be an essential development-associated factor in Drosophila. To probe the possibility that it contributes to hemocyte development, we used a collagen promoter-GAL4 strain to over-express dsRNA of D-DDB1 in Drosophila hemocytes. The D-DDB1 gene silencing caused melanotic tumors and mortality at the end of larval development. Similarly, it interfered with melanization and synthesis of antimicrobial peptides. Transgenic flies with D-DDB1 gene silencing were found to accumulate abnormal large blood cells, reminiscent of human leukemia, suggesting that D-DDB1 has functions in hemocyte development.
authors.affiliation: Department of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, Noda-shi, Chiba-ken 278-8510, Japan.
authors.forename: Kei-ichi
authors.initials: K
authors.lastname: Takata
authors.forename: Kaori
authors.initials: K
authors.lastname: Shimanouchi
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Shizuka
authors.initials: S
authors.lastname: Murakami
authors.forename: Gen
authors.initials: G
authors.lastname: Ishikawa
authors.forename: Ryo
authors.initials: R
authors.lastname: Takeuchi
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Kanai
authors.forename: Tatsushi
authors.initials: T
authors.lastname: Ruike
authors.forename: Ryou-ichi
authors.initials: R
authors.lastname: Nakamura
authors.forename: Yoko
authors.initials: Y
authors.lastname: Abe
authors.forename: Kengo
authors.initials: K
authors.lastname: Sakaguchi
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000172:deficiency* / Q000235:genetics / Q000276:immunology*; D004330:Drosophila / Q000166:cytology / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D029721:Drosophila Proteins / Q000172:deficiency* / Q000235:genetics / Q000276:immunology*; D004706:Endodeoxyribonucleases / Q000172:deficiency* / Q000235:genetics / Q000276:immunology*; D006434:Hemocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D007113:Immunity, Innate / Q000276:immunology; D007938:Leukemia / Q000276:immunology* / Q000378:metabolism*; D009928:Organ Specificity; D011994:Recombinant Proteins / Q000276:immunology / Q000378:metabolism; D014018:Tissue Distribution
chemical_list: D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D011994:Recombinant Proteins; D004706:Endodeoxyribonucleases; C112206:DdbP1 protein, Drosophila