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Gene Review

AttA  -  Attacin-A

Drosophila melanogaster

Synonyms: ATT, Att, Att A, Att-A, BcDNA:LP05763, ...
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Disease relevance of AttA

  • This accumulation of DNA in the DNase II mutants caused the constitutive expression of the antibacterial genes for diptericin and attacin, which are usually activated during bacterial infection [1].
  • In all, 6713 dsRNAs from an S2 cell-derived cDNA library were analyzed for their effect on Attacin promoter activity in response to Escherichia coli [2].

High impact information on AttA

  • This binding led to recruitment of the histone deacetylase dHDAC1 to the promoter of the gene encoding the antibacterial protein Attacin-A and to local modification of histone acetylation content [3].
  • We identified seven gene products required for the Attacin response in vitro, including two novel Imd pathway components: inhibitor of apoptosis 2 (Iap2) and transforming growth factor-activated kinase 1 (TAK1)-binding protein (TAB) [2].
  • Induction of Attacin A by Geotrichum candidum required Relish, whereas activation by Beauvaria bassiana required Dif, suggesting that the Drosophila immune system can distinguish between at least these two fungi [4].
  • Through GmmRel knock-down, we could successfully block the induction of attacin and cecropin expression in the immune responsive tissues fat body and proventriculus (cardia) following microbial challenge [5].
  • The midgut and salivary gland trypanosome infection prevalence, as well as the intensity of midgut parasite infections were found to be significantly higher in flies when attacin and relish expression were knocked down [5].

Biological context of AttA

  • The corresponding Attacin A (Att A) gene is localized at 51A-B on the second chromosome, and it is closely linked to at least one more cross-hybridizing gene [6].
  • We present a comparison of the promoter regions of the two attacin genes to those cloned from other antimicrobial peptide genes to assist a better understanding of how antimicrobial genes are differentially regulated [7].
  • The number and organization of binding sites for kappaB and other transcription factors in the promoter regions of both attacin genes are consistent with strong and rapid immune induction [7].

Other interactions of AttA


  1. Activation of the innate immunity in Drosophila by endogenous chromosomal DNA that escaped apoptotic degradation. Mukae, N., Yokoyama, H., Yokokura, T., Sakoyama, Y., Nagata, S. Genes Dev. (2002) [Pubmed]
  2. Inhibitor of apoptosis 2 and TAK1-binding protein are components of the Drosophila Imd pathway. Kleino, A., Valanne, S., Ulvila, J., Kallio, J., Myllymäki, H., Enwald, H., Stöven, S., Poidevin, M., Ueda, R., Hultmark, D., Lemaitre, B., Rämet, M. EMBO J. (2005) [Pubmed]
  3. Downregulation of lipopolysaccharide response in Drosophila by negative crosstalk between the AP1 and NF-kappaB signaling modules. Kim, T., Yoon, J., Cho, H., Lee, W.B., Kim, J., Song, Y.H., Kim, S.N., Yoon, J.H., Kim-Ha, J., Kim, Y.J. Nat. Immunol. (2005) [Pubmed]
  4. Differential activation of the NF-kappaB-like factors Relish and Dif in Drosophila melanogaster by fungi and Gram-positive bacteria. Hedengren-Olcott, M., Olcott, M.C., Mooney, D.T., Ekengren, S., Geller, B.L., Taylor, B.J. J. Biol. Chem. (2004) [Pubmed]
  5. Innate immune responses regulate trypanosome parasite infection of the tsetse fly Glossina morsitans morsitans. Hu, C., Aksoy, S. Mol. Microbiol. (2006) [Pubmed]
  6. Identification of early genes in the Drosophila immune response by PCR-based differential display: the Attacin A gene and the evolution of attacin-like proteins. Asling, B., Dushay, M.S., Hultmark, D. Insect Biochem. Mol. Biol. (1995) [Pubmed]
  7. Two attacin antibacterial genes of Drosophila melanogaster. Dushay, M.S., Roethele, J.B., Chaverri, J.M., Dulek, D.E., Syed, S.K., Kitami, T., Eldon, E.D. Gene (2000) [Pubmed]
  8. Expression and evolution of the Drosophila attacin/diptericin gene family. Hedengren, M., Borge, K., Hultmark, D. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  9. Drosophila melanogaster is susceptible to Vibrio cholerae infection. Park, S.Y., Heo, Y.J., Kim, K.S., Cho, Y.H. Mol. Cells (2005) [Pubmed]
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