ArticleMolecular and cellular biology2010
The POU transcription factor Drifter/Ventral veinless regulates expression of Drosophila immune defense genes.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 58 citations in OpenAlex.
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- Shared Transcriptomic Signatures of Inflammaging Among Diverse Strains of Drosophila melanogaster.Research square · 2024Article
- Comparative transcriptome analysis of whiteflies raised onFrontiers in veterinary science · 2024Article
- Single-nucleus transcriptomes reveal evolutionary and functional properties of cell types in the Drosophila accessory gland.Genetics · 2022Article
- Regulatory regions in natural transposable element insertions drive interindividual differences in response to immune challenges in Drosophila.Genome biology · 2021Article
- Stop codon readthrough alters the activity of a POU/Oct transcription factor during Drosophila development.BMC biology · 2021Article
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- The POU Transcription Factor POU-M2 RegulatesGenes · 2020Article
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- Crossveinless is a direct transcriptional target of Trachealess and Tango in Drosophila tracheal precursor cells.PloS one · 2019Article
- Sexual Dimorphisms in Innate Immunity and Responses to Infection inFrontiers in immunology · 2019Review
- Insect Transcription Factors: A Landscape of Their Structures and Biological Functions inInternational journal of molecular sciences · 2018Review
- Evolutionary plasticity in the innate immune function of Akirin.PLoS genetics · 2018Article
- Genome-wide identification of Grainy head targets inDevelopment (Cambridge, England) · 2017Article
- Transcriptional control of steroid biosynthesis genes in the Drosophila prothoracic gland by ventral veins lacking and knirps.PLoS genetics · 2014Article
- The Drosophila IMD pathway in the activation of the humoral immune response.Developmental and comparative immunology · 2014Review
- Article
- The Oct1 homolog Nubbin is a repressor of NF-κB-dependent immune gene expression that increases the tolerance to gut microbiota.BMC biology · 2013Article
- Inhibition of the binding of MSG-intermolt-specific complex, MIC, to the sericin-1 gene promoter and sericin-1 gene expression by POU-M1/SGF-3.Development genes and evolution · 2012Article
- Drosophila as a model system to unravel the layers of innate immunity to infection.Open biology · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate immunity operates as a first line of defense in multicellular organisms against infections caused by different classes of microorganisms. Antimicrobial peptides (AMPs) are synthesized constitutively in barrier epithelia to protect against microbial attack and are also upregulated in response to infection. Here, we implicate Drifter/Ventral veinless (Dfr/Vvl), a class III POU domain transcription factor, in tissue-specific regulation of the innate immune defense of Drosophila. We show that Dfr/Vvl is highly expressed in a range of immunocompetent tissues, including the male ejaculatory duct, where its presence overlaps with and drives the expression of cecropin, a potent broad-spectrum AMP. Dfr/Vvl overexpression activates transcription of several AMP genes in uninfected flies in a Toll pathway- and Imd pathway-independent manner. Dfr/Vvl activates a CecA1 reporter gene both in vitro and in vivo by binding to an upstream enhancer specific for the male ejaculatory duct. Further, Dfr/Vvl and the homeodomain protein Caudal (Cad) activate transcription synergistically via this enhancer. We propose that the POU protein Dfr/Vvl acts together with other regulators in a combinatorial manner to control constitutive AMP gene expression in a gene-, tissue-, and sex-specific manner, thus promoting a first-line defense against infection in tissues that are readily exposed to pathogens.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.