We characterized monosaccharide-dependent gene expression in the Drosophila fat body using fructose and glucose. Control and high-sugar diets were compared and RNA-seq was used to identify potential target genes. Overall design: Drosophila were reared on control (0.3 M fructose or glucose) or high sugar (1.7 M fructose or glucose) diets until the wandering third instar stage. Fat bodies were isolated and RNA was extracted to determine the effects of each sugar at different concentrations on gene expression using Illumina RNA-seq.
Similar effects of high-fructose and high-glucose feeding in a Drosophila model of obesity and diabetes.
Sex, Specimen part, Cell line, Subject
View SamplesWe compared gene expression in the Drosophila fat body on control and high-sugar diets in order to gain insight into the role of this organ during caloric overload. Differential expression analysis revealed changes in gene expression suggestive of a role for CoA metabolism in the ability to tolerate high-sugar feeding. This led us to perform biochemical and mutant studies supporting a model where CoA is limiting in the face of caloric overload. Overall design: Wild-type Drosophila were reared on control (0.15M sucrose) and high-sugar (0.7M sucrose) diets until the wandering stage. Fat bodies were isolated and RNA extracted to determine the effects of diet on gene expression using Illumina RNA-seq.
CoA protects against the deleterious effects of caloric overload in Drosophila.
Sex, Specimen part, Subject
View SamplesWe compared four transcription factor knockdowns using transgenic RNAi expressed in the larval fat body. FOXO, Tfb1, p53, and Stat92E-dependent gene expression in the Drosophila fat body was quantified on control and high-sugar diets in order to generate expression profiles via RNA-seq. These expression data were used to build a gene regulatory network to predict novel roles for these and other genes during caloric overload. Overall design: Control and fat body-expressed transcription factor RNAi Drosophila were reared on control (0.15M sucrose) and high-sugar (0.7M or 1M sucrose) diets until the wandering stage. Fat bodies were isolated and RNA extracted to determine the effects of diet on gene expression using Illumina RNA-seq.
Seven-Up Is a Novel Regulator of Insulin Signaling.
Sex, Specimen part, Treatment, Subject
View SamplesChronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. These phenotypes are controlled by the fat body, a liver- and adipose- like tissue in Drosophila flies. To gain insight into the mechanisms underlying the connection between diet and insulin sensitivity, we used Illumina RNA-seq to profile gene expression in fat bodies isolated from chronically high sugar fed, wandering (post-prandial) third instar wild type larvae w(L3). These data were compared to control-fed wild-type wL3 fat bodies as well as those expressing transgenic interfering RNA (i) targeting CG18362 (Mio/dChREBP) in the fat body on both diets. Overall design: Female VDRC w1118, cgGAL4, UAS-Dcr2 or UAS-ChREBPi(52606), cgGAL4, UAS-Dcr2 wandering third instar larvae were fed control (0.15M) or high (0.7M) sucrose and fat bodies isolated for RNA extraction.
Seven-Up Is a Novel Regulator of Insulin Signaling.
Sex, Specimen part, Subject
View SamplesWe compared ecdysone receptor (EcR)-dependent gene expression in the Drosophila fat body on 0.15 M sucrose and 0.5 M sucrose high-sugar diets in order to gain insight into the role of this gene during caloric overload. Phenotypic analyses showed an increased severity of EcR RNAi phenotypes with increasing dietary sugar concentration. Because EcR is a transcription factor, we performed RNA-seq studies to identify transcriptional targets that might underlie insulin resistance downstream of EcR RNAi. Overall design: Control and fat body-expressed EcR RNAi Drosophila were reared on control (0.15 M sucrose) and high-sugar (0.5 M sucrose) diets until the wandering stage. Fat bodies were isolated and RNA extracted to determine the effects of diet on gene expression using Illumina RNA-seq.
Seven-Up Is a Novel Regulator of Insulin Signaling.
Sex, Specimen part, Subject
View SamplesWe compared Seven-up-dependent gene expression in the Drosophila fat body on control and high-sugar diets in order to gain insight into the role of this gene during caloric overload. Phenotypic analyses showed an increased severity of Seven-up RNAi phenotypes with increasing dietary sugar concentration. Because Seven-up is a transcription factor, we performed RNA-seq studies to identify transcriptional targets that might underlie insulin resistance downstream of Seven-up RNAi. Our data support a model where Seven-up promotes insulin signaling by inhibiting ecdysone receptor target gene expression. Overall design: Control and fat body-expressed Seven-up RNAi Drosophila were reared on control (0.15M sucrose) and high-sugar (0.7M sucrose) diets until the wandering stage. Fat bodies were isolated and RNA extracted to determine the effects of diet on gene expression using Illumina RNA-seq.
Seven-Up Is a Novel Regulator of Insulin Signaling.
Sex, Specimen part, Subject
View SamplesIn order to identify genes dysregulated by the aberrant transcriptional activity of RUNX1-RUNX1T1, we used microarrays to determine the effect of this mutation on gene expression during myeloid and erythroid development of normal human progenitor cells.
Transcriptional dysregulation mediated by RUNX1-RUNX1T1 in normal human progenitor cells and in acute myeloid leukaemia.
Specimen part
View SamplesChronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. To gain insight into the mechanisms underlying this response, we profiled gene expression in chronically high sugar fed, wandering (post-prandial) third instar wild type larvae (L3). These data were compared to control-fed larvae as well as those (mid-L3) actively feeding for twelve hours on both diets.
A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila.
Sex, Specimen part
View SamplesChronic high-sugar feeding (1 M or 34% sucrose) leads to hyperglycemia, obesity, and insulin resistance in adult flies, compared with those fed a control diet (0.15 M or 5% sucrose). We compared two days and four weeks of high-sugar feeding to look at short- and long- term effects on gene expression.
A Complex Relationship between Immunity and Metabolism in Drosophila Diet-Induced Insulin Resistance.
Sex
View SamplesWe characterized insulin receptor (InR)-dependent gene expression in the Drosophila fat body using transgenic RNAi. Chronic knockdown of InR in the fat body was elicited via (r4-GAL4, UAS-InRi) and RNA-seq was used to identify potential target genes. Overall design: Drosophila were reared on control (0.15 M sucrose) or high sugar (0.7 M sucrose) diets until the wandering third instar stage. Control (r4-GAL4 x w1118) offspring were compared with InRi (r4-GAL4 x UAS-InRi) using the VDRC''s w1118 (#60000) or UAS-RNAi targeting InR (#992). Fat bodies were isolated, and RNA was extracted to determine the effects of reduced insulin signaling on gene expression using Illumina RNA-seq.
A Complex Relationship between Immunity and Metabolism in Drosophila Diet-Induced Insulin Resistance.
Sex, Specimen part, Treatment, Subject
View Samples