Project description:Loss of Ck1alpha produces 'flyabetic' larvae that are feeding defective. In addition we found other larvae with glucose elevations show feeding aversion. We performed microarray to identify potential candidates that are involved in glucose-regulated feeding behaviors
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.
Project description:Maternal obesity and diabetes is associated with increased risk of obesity and diabetes in offspring. We generated a model of maternal caloric excess in Drosophila and noted altered body composition in offspring from females fed a high-sucrose diet. To gain insight into the mechanisms underlying this response, we profiled gene expression in mid-third instar larvae (mid-L3) offspring from either control or high-sucrose fed females. All offspring were raised on control food. We used microarrays to detail the response of Drosophila larvae to maternal high calorie diet
Project description:We report here the transcriptomic analysis of Drosophila melanogaster wing imaginal discs from third instar female larvae mutant for corto (cortoL1/corto420) The reference line was the w1118 genetic background of the mutant lines.
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. Male Canton-S third instar larvae were fed control (0.15M) or high (1M) sucrose and selected for RNA extraction and hybridization on Affymetrix microarrays. Wandering L3 were selected as those in the top half of the vial with partial blue guts to confirm that they had stopped eating the (blue) food. Mid-L3 were selected as L2, aged overnight until early L3, then transferred to fresh control or high sucrose food for 12 more hours before selection.
Project description:Maternal obesity and diabetes is associated with increased risk of obesity and diabetes in offspring. We generated a model of maternal caloric excess in Drosophila and noted altered body composition in offspring from females fed a high-sucrose diet. To gain insight into the mechanisms underlying this response, we profiled gene expression in mid-third instar larvae (mid-L3) offspring from either control or high-sucrose fed females. All offspring were raised on control food. We used microarrays to detail the response of Drosophila larvae to maternal high calorie diet Virgin female w1118 flies were fed control (0.15M) or high (1M) sucrose food for 7 days, mated with male w1118 flies such that all embryos were laid on control food. Mid-L3 larvae were selected for RNA extraction and hybridization on Affymetrix microarrays. Mid-L3 were selected as L2, aged overnight until early L3, then transferred to fresh control food for 12 more hours before selection.
Project description:Ectopic expression of DNMT3L in Drosophila causes melanotic tumor in the transgenic flies from fifth generation onwards. We used microaarray data analysis to look for the genes and pathways which are affected on ectopic expression of DNMT3L in Drosophila. Drosophila third instar larvae were selected at particular stages of development for RNA extraction and hybridization on Affymetrix microarrays.
Project description:We report here the transcriptomic analysis of Drosophila melanogaster wing imaginal discs from third instar female larvae expressing Cyclin G deleted of the PEST domain (the 25 COOH-terminal amin-acids) under the control of the daugterless-Gal4 ubiquitous driver. The negative control was transgenic flies wearing only the daugterless-Gal4 driver.
Project description:Our data on third instar larvae tissues of Drosophila melanogaster has allowed us to identify bsAS, a lncRNA antisense to the blistered/DSRF gene, orthologous to the SRF transcription factor in humans, mainly expressed in fly wings. bsAS controls the expression of different isoforms of the blistered gene in Drosophila tissues. CRISPR-CAS deletion of bsAS Transcription Start Site thoroughly abolishes bsAS transcription, inducing a change in the bs isoform usage and the impairment of wing development. Our data consists on stranded RNA-Seq from eye-antenna, leg and wing imaginal discs from third instar larvae. To analyse bsAS mutation, we also performed stranded RNA-Seq of wild type and bsAS-/- eyes and wings from third instar larvae and late pupae.