Although host genetics influences susceptibility to tuberculosis, few genes determining disease outcome have been identified. We hypothesized that macrophages from individuals with different clinical manifestations of tuberculosis infection would have distinct gene expression profiles, and that polymorphisms in these genes may also be associated with susceptibility to TB.
Identification of tuberculosis susceptibility genes with human macrophage gene expression profiles.
No sample metadata fields
View SamplesHere we study the adult functions of the single Drosophila member of this subfamily, DHR78, with the goal of defining its ancestral functions in the absence of genetic redundancy. We show that DHR78 mutants have a shortened lifespan and reduced motility. Mated DHR78 mutant females display reduced triglycerides along with a reduced feeding rate. Transcriptional profiling reveals a major role for DHR78 in promoting the expression of genes that are abundantly expressed in the midgut, suggesting that it contributes to nutrient uptake. We also identify roles for DHR78 in maintaining the expression of genes in the ecdysone and Notch signaling pathways. Overall design: Comparison of the transcriptional profile of DHR78-transheterozygote female mutants in a btl>DHR78 background with genetically matched controls
Adult functions for the Drosophila DHR78 nuclear receptor.
Sex, Age, Specimen part, Subject
View SamplesAlthough SIRT1 plays a central role in maintaining metabolic homeostasis, the molecular mechanisms remain unclear. Here we show that loss of the Drosophila SIRT1 homolog sir2 leads to the progressive onset of diabetic phenotypes, similar to studies of SIRT1 in mice. Sir2 function is both necessary and sufficient in the fat body to maintain peripheral insulin sensitivity. This activity is mediated by the Drosophila HNF4 nuclear receptor, which is deacetylated and stabilized through protein interactions with Sir2. This study demonstrates that the key metabolic activities of SIRT1 have been conserved through evolution and establishes HNF4 as a critical downstream target. Overall design: 4 sir2 mutant, 4 control samples, independent biological replicates
Sir2 Acts through Hepatocyte Nuclear Factor 4 to maintain insulin Signaling and Metabolic Homeostasis in Drosophila.
Age, Subject
View SamplesThere is a good deal of indirect evidence that improved insulin sensitivity may contribute to improved lifespan of mice in which aging has been slowed by mutations, drugs, or dietary means, even in stocks of mice that do not show signs of late-life diabetes. Peripheral responses to insulin can be augmented by over-expression of Syntaxin 4 (Syn4), a membrane SNARE protein. We show here that Syn4 transgenic (Tg) mice live approximately 33% longer than controls, and show increased peripheral insulin sensitivity, even at ages where controls show age-related insulin resistance. Hence, presumably Syn4 Tg mice spend more hours of each day under normoglycemic conditions, which may slow multiple aspects of aging and thereby extend lifespan, even in non-diabetic mice.
Syntaxin 4 Overexpression Ameliorates Effects of Aging and High-Fat Diet on Glucose Control and Extends Lifespan.
Sex, Specimen part
View SamplesThis study identifies genes that alter their expression in synchrony with the late third instar and prepupal pulses of 20E.
The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis.
No sample metadata fields
View SamplesThis study identifies those genes that are dependent on EcR for their proper regulation at the onset of metamorphosis in Drosophila melanogaster.
The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis.
No sample metadata fields
View SamplesTo identify 20E-regulated genes, wandering third instar larvae were dissected and their organs were cultured in the presence of either no hormone, 20E alone, cycloheximide alone, or 20E plus cycloheximide for six hours.
The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis.
No sample metadata fields
View SamplesPhenobarbital is a well studied xenobiotic compound. In this study, we describe the genomic responses in fruit flies and examine whether animals mutant for DHR96, an ortholog of xenobiotic nuclear receptors PXR and CAR, plays a role in mediating xenobiotic responses in Drosophila.
The DHR96 nuclear receptor regulates xenobiotic responses in Drosophila.
No sample metadata fields
View SamplesTransgenerational effects of parental metabolic state have been shown, but the mechanism is still unclear. Here we present transcriptome sequencing data from AKHR heterozygous F1 progeny, either from obese maternal or paternal parents, compared to genetically matched heterozygous controls or to wild-type controls Overall design: 3 AKHR heterozygous samples descended from obese maternal parents, 3 AKHR heterozygous samples descended from obese paternal parents, 3 AKHR heterozygous samples descended from non-obese parents, and 3 wild-type controls, independent biological replicates and independent experimental replicates (1 set of samples from each experimental replicate)
Parental obesity leads to metabolic changes in the F2 generation in <i>Drosophila</i>.
Specimen part, Subject
View SamplesDHR96 plays a role in regulating xenobiotic responses in Drosophila. Using a gain-of-function approach we test whether DHR96 is sufficient to affect detoxification genes in the absence of a xenobiotic insult.
The DHR96 nuclear receptor regulates xenobiotic responses in Drosophila.
No sample metadata fields
View Samples