Project description:We used RNA-seq in a derived European Drosophila melanogaster population from Germany (MU) to examine coding gene expression variation in the larval fat body during the late wandering third instar stage.
Project description:Chronic 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. 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.
Project description:Chronic 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.
Project description:We use mRNA-seq to transcriptionally profile larval fat body and midgut tissues from Drosophila third instar larvae. These data provide insights into tissue physiology and can be used to identify tissue specific transcripts. Fat bodies from wandering third instar larvae were dissected from ~50 male larvae and gonads were removed to eliminate contaminating transctips from the gonads. Larval midguts were dissected from ~50 wandering third instar larvae. Larval tissues were removed to Graces unsupplemented medium on ice prior to RNA extraction with TRIzol reagent. mRNA-seq samples were prepared from 5ug of total RNA and subject to Illumina based sequencing.
Project description:To identify genes differentially expressed in the fatbody of Drosphila melanogaster bigmax mutants, a loss-of-function allele was generated by P-element mobilization. Mutant and wildtype first instar larvae were raised on two different sources of food, control and high-sugar media. When the animals reached the wandering third instar stage, animals were sacrificed and their fat bodies dissected. Total RNA was extracted, labeled fluorescently and hybridized competitively to Agilent's 4x44K Drosophila Gene Expression Microarrays. On each array, three different samples were analyzed: 1. wildtype animals raised on control food, 2. wildtype animals raised on high-sugar food and 3. bigmax mutant animals raised on high-sugar food.
Project description:Chronic 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. We used microarrays to detail the response of Drosophila larvae to high sugar-induced insulin resistance.
