Project description:We found in our behavior experiment clearly distinnct olfactory responses in fed vs starved flies in response to differrent odors.To investigate the molecular basis of the starvation mediated olfactory modulation process, we compared gene expression at the level of the antenna and the brain for fed and starved flies.
Project description:Oral food intake maintains gastrointestinal cell turnover and impacts the morphology and function of intestinal epithelial cells. However, the underlying mechanism is not fully elucidated, especially in the large intestine. Therefore, we analyzed the colonic epithelial cell turnover in starved and re-fed mice.
Project description:We found in our behavior experiment clearly distinnct olfactory responses in fed vs starved flies in response to differrent odors.To investigate the molecular basis of the starvation mediated olfactory modulation process, we compared gene expression at the level of the antenna and the brain for fed and starved flies. Gene expression in brain and antennae was measured at 0hr and 28 hours starved. Four independent experiments were performed at each time using different flies for each experiment.
Project description:N2 worms were subjected to control (well-fed), short-term dauer (6 d), or long-term dauer (40 - 49 d) conditions. Worms were recovered and maintained well-fed for 3 generations. F3 progeny were collected as fed or starved L1 larvae.
Project description:We show that dHNF4 null mutant larvae are sensitive to starvation. Starved mutant larvae consume glycogen normally, but retain lipids in their midgut and fat body, and have increased levels of long chain fatty acids, suggesting that they are unable to efficiently mobilize stored fat for energy. HNF4 dependent transcripts were identified under fed and starved conditions. Microarray studies indicate reduced expression of genes that control lipid catabolism and ï¢-oxidation. Late second instar control and HNF4 mutant larvae were collected and fed or starved for 24 hours, and then RNA was isolated for analysis. Taken together, our results support a feed-forward model for dHNF4, in which fatty acids released from triglycerides activate the receptor, inducing enzymes that drive fatty acid oxidation for energy production. Experiment Overall Design: Staged late second instar control larvae that were transheterozygous for precise excisions of the EP2449 and KG08976 P-elements, and dHNF4D33/dHNF4D17 mutant larvae, were either fed or starved for 24 hrs in a 55mm petri dish containing Whatman paper soaked with PBS. RNA was extracted from the apparently healthy animals that molted to the third instar using Trizol (Gibco) and purified on RNAeasy columns (Qiagen). All samples were prepared in triplicate to facilitate subsequent statistical analysis. Probe labeling, hybridization to Affymetrix GeneChip® Drosophila Genome 2.0 Arrays.