Interaction and Specificity of Rel-related Proteins in Regulating Drosophila Immunity Gene Expression

Han, Zhiqiang; Ip, Y. Tony

doi:10.1074/jbc.274.30.21355

Cited by 104 publications

(112 citation statements)

References 41 publications

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“…IKK immunoprecipitation kinase assays were performed as described previously, except that 100 ng of recombinant baculovirus-produced Relish was used. For baculovirus construction, FLAG Relish from pSH-Relish (29) was cloned into the shuttle vector pHIS-BIVT (30). JNK signaling activity was monitored with a c-Jun shift assay, as described previously (31).…”

Section: Methodsmentioning

confidence: 99%

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Silverman

Zhou²,

Erlich

et al. 2003

Journal of Biological Chemistry

236

230

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Section: Methodsmentioning

confidence: 99%

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Silverman

Zhou²,

Erlich

et al. 2003

Journal of Biological Chemistry

236

230

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“…The target enhancers may be bound by homodimers and/or heterodimers of the three NF-kB proteins. For example, the enhancer of the immune peptide gene drosomycin contains kB-elements that can be bound by both Dorsal/ Dif and Relish (Han and Ip, 1999). Thus the transcription factors may cooperatively regulate several immune peptide genes.…”

Section: The Imd Pathway and The Drosophila Immune Responsementioning

confidence: 99%

Nuclear factor-kappa B pathways in Drosophila

Minakhina

Steward

2006

Oncogene

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“…T ranscriptional regulation of Drosophila antimicrobial genes depends on Rel and GATA transcription factors (1)(2)(3)(4)(5)(6). Many immunity genes contain tightly linked Rel-and GATAbinding sites in promoter-proximal regions.…”

mentioning

confidence: 99%

DEAF-1 regulates immunity gene expression in Drosophila

Reed

Huang

Wohlschlegel

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Immunity genes are activated in the Drosophila fat body by Rel and GATA transcription factors. Here, we present evidence that an additional regulatory factor, deformed epidermal autoregulatory factor-1 (DEAF-1), also contributes to the immune response and is specifically important for the induction of two genes encoding antimicrobial peptides, Metchnikowin (Mtk) and Drosomycin (Drs). The systematic mutagenesis of a minimal Mtk 5 enhancer identified a sequence motif essential for both a response to LPS preparations in S2 cells and activation in the larval fat body in response to bacterial infection. Using affinity chromatography coupled to multidimensional protein identification technology (MudPIT), we identified DEAF-1 as a candidate regulator. DEAF-1 activates the expression of Mtk and Drs promoter-luciferase fusion genes in S2 cells. SELEX assays and footprinting data indicate that DEAF-1 binds to and activates Mtk and Drs regulatory DNAs via a TTCGGBT motif. The insertion of this motif into the Diptericin (Dpt) regulatory region confers DEAF-1 responsiveness to this normally DEAF-1-independent enhancer. The coexpression of DEAF-1 with Dorsal, Dif, and Relish results in the synergistic activation of transcription. We propose that DEAF-1 is a regulator of Drosophila immunity.T ranscriptional regulation of Drosophila antimicrobial genes depends on Rel and GATA transcription factors (1-6). Many immunity genes contain tightly linked Rel-and GATAbinding sites in promoter-proximal regions. GATA sites are important for establishing responses in distinct tissues such as the fat body and midgut. Serpent (dGATAb) is thought to regulate antimicrobial gene expression in the fat body (7, 8), whereas dGATAe activates such genes in the midgut in response to ingested microbes (9). In contrast, Dorsal, Dif, and Relish, the NF-B homologues in flies, shuttle between the cytoplasmic and nuclear compartments, acting as ''on/off switches'' for induction (10)(11)(12). Additional factors, such as HOX and POU domain proteins, bind to distal enhancer elements and maintain constitutive domains of gene activity (13). A regulatory element (R1) also has been described within the CecA1 enhancer (14), although the factor that interacts with this motif is unknown.Deformed epidermal autoregulatory factor-1 (DEAF-1) is a transcription factor that was originally shown to bind the autoregulatory enhancer of the Deformed (Dfd) Hox gene, which is activated in embryonic head segments of Drosophila (15). DEAF-1 recognizes several TTCG motifs within the portion of the Dfd autoregulatory region termed ''module E.'' In addition, DEAF-1 binds several similar motifs within a Dfd response element (DRE) from the 1.28 gene that enhances maxillary gene expression during embryogenesis (16). The DEAF-1 binding elements identified in these studies are reportedly not required for enhancer activity however (16,17).The 576-aa DEAF-1 protein possesses two conserved domains, SAND and MYND. The 113-aa SAND domain (named for SP100, AIRE-1, NucP41/75, and DEAF-1) (18) i...

show abstract

Interaction and Specificity of Rel-related Proteins in Regulating Drosophila Immunity Gene Expression

Cited by 104 publications

References 41 publications

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Immune Activation of NF-κB and JNK Requires Drosophila TAK1

Nuclear factor-kappa B pathways in Drosophila

DEAF-1 regulates immunity gene expression in Drosophila

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