Reference Report

Reference
Citation	Leulier, F., Lhocine, N., Lemaitre, B., Meier, P. (2006). The Drosophila inhibitor of apoptosis protein DIAP2 functions in innate immunity and is essential to resist gram-negative bacterial infection. Mol. Cell. Biol. 26(21): 7821--7831. (Export to RIS)
FlyBase ID	FBrf0192381
Publication Type	Research paper
PubMed ID	16894030
PubMed Abstract	The founding member of the inhibitor of apoptosis protein (IAP) family was originally identified as a cell death inhibitor. However, recent evidence suggests that IAPs are multifunctional signaling devices that influence diverse biological processes. To investigate the in vivo function of Drosophila melanogaster IAP2, we have generated diap2 null alleles. diap2 mutant animals develop normally and are fully viable, suggesting that diap2 is dispensable for proper development. However, these animals were acutely sensitive to infection by gram-negative bacteria. In Drosophila, infection by gram-negative bacteria triggers the innate immune response by activating the immune deficiency (imd) signaling cascade, a NF-kappaB-dependent pathway that shares striking similarities with the pathway of mammalian tumor necrosis factor receptor 1 (TNFR1). diap2 mutant flies failed to activate NF-kappaB-mediated expression of antibacterial peptide genes and, consequently, rapidly succumbed to bacterial infection. Our genetic epistasis analysis places diap2 downstream of or in parallel to imd, Dredd, Tak1, and Relish. Therefore, DIAP2 functions in the host immune response to gram-negative bacteria. In contrast, we find that the Drosophila TNFR-associated factor (Traf) family member Traf2 is dispensable in resistance to gram-negative bacterial infection. Taken together, our genetic data identify DIAP2 as an essential component of the Imd signaling cascade, protecting the organism from infiltrating microbes.
DOI	10.1128/MCB.00548-06
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Mol. Cell. Biol.
Title	Molecular and Cellular Biology
Publication Year	1981-
ISBN/ISSN	0270-7306
Data from Reference
Aberrations (1)
	Df(2R)Exel7138
Alleles (15)
	Dredd^Scer\UAS.cVa Iap2^7a Iap2^7c Iap2^G2326 Iap2^Scer\UAS.cLa imd^Scer\UAS.cGa Rel^E20 Rel^{Scer\UAS.T:Zzzz\His6} Scer\GAL4^Act5C.PU Scer\GAL4^da.G32 Scer\GAL4^hs.PB spz⁴ Tak1¹ Tak1^Scer\UAS.cTa Traf6^ex1
Constructs (7)
	P{Act5C-GAL4.U} P{GAL4-da.G32} P{UAS-Dredd.V} P{UAS-Iap2.L} P{UAS-imd.G} P{UAS-Rel.His6} P{UAS-Tak1}
Genes (16)
	AttA CecA1 Def Dpt Dredd Dro Drs Iap2 imd Mtk Rel Scer\GAL4 spz Tak1 th Traf6
Insertions (1)
	P{EP}Iap2^G2326