Dataset Information

Mating regulates growth, metabolism, and digestive efficiency in the female Drosophila midgut

ABSTRACT: Adaptive changes in organ size and function occur in most animals, but how these changes are regulated is not well understood. Previous research found that mating in Drosophila females promotes intestinal stem cell proliferation and increases the overall size of the endodermal portion of the intestine (the “midgut”). Other studies reported mating-dependent changes in feeding behavior, midgut gene expression, and whole-body lipid storage, suggesting altered metabolism. Here, we show that mating dramatically alters female midgut metabolism and digestive function. Mating increased relative levels of TCA cycle intermediates, fatty acids, and ceramides in the gut, increased total midgut lipids and protein, and reduced relative carbohydrate levels. Mating also enhanced the efficiency of protein digestion relative to carbohydrate digestion. Corroborating a previous report, we found that the expression of genes tha mediate protein and carbohydrate and metabolism was similarly altered. In addition, we noted a mating-dependent downregulation of oxidative stress response and autophagy genes. Mating-dependent increases in ecdysone receptor (EcR) signaling were important for increasing TCA cycle intermediates, protein, and ceramides in the female midgut, but had minimal effects on bulk lipid accumulation. Overall, this study contributes to our understanding of the physiological changes that occur during adaptive intestinal growth, and how they are regulated.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE315594 | GEO | 2026/01/05

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Carbohydrate Response Element-Binding Protein (ChREBP) is a transcription factor that activates key genes involved in glucose, fructose, and lipid metabolism in response to carbohydrate feeding, but its other potential roles in metabolic homeostasis have not been as well studied. We used liver-selective GalNAc-siRNA technology to suppress expression of ChREBP in rats fed a high fat/high sucrose diet and characterized hepatic and systemic responses by integrating transcriptomic and metabolomic analyses. GalNAc-siChREBP-treated rats had lower levels of multiple short-chain acyl CoA metabolites compared to rats treated with GalNAc-siCtrl containing a non-targeting siRNA sequence. These changes were related to a sharp decrease in free CoA levels in GalNAc-siChREBP treated-rats, accompanied by lower expression of transcripts encoding enzymes and transporters involved in CoA biosynthesis. These activities of ChREBP likely contribute to its complex effects on hepatic lipid and energy metabolism. While core enzymes of fatty acid (FA) oxidation are induced by ChREBP knockdown, accumulation of liver acylcarnitines and circulating ketones indicate diversion of acetyl CoA to ketone production rather than complete oxidation in the TCA cycle. Despite strong suppression of pyruvate kinase and activation of pyruvate dehydrogenase, pyruvate levels were maintained, likely via increased expression of pyruvate transporters, and decreased expression of lactate dehydrogenase and alanine transaminase. GalNAc-siChREBP treatment increased hepatic citrate and isocitrate levels while decreasing levels of distal TCA cycle intermediates. The drop in free CoA levels, needed for the 2-ketoglutarate dehydrogenase reaction, as well as a decrease in transcripts encoding the anaplerotic enzymes pyruvate carboxylase, glutamate dehydrogenase, and aspartate transaminase likely contributed to these effects. GalNAc-siChREBP treatment caused striking increases in PRPP and ZMP/AICAR levels, and decreases in GMP, IMP, AMP, NaNM, NAD(P), and NAD(P)H levels, accompanied by reduced expression of enzymes that catalyze late steps in purine and NAD synthesis. ChREBP suppression also increased expression of a set of plasma membrane amino acid transporters, possibly as an attempt to replenish TCA cycle intermediates. In sum, combining transcriptomic and metabolomic analyses has revealed regulatory functions of ChREBP that go well beyond its canonical roles in control of carbohydrate and lipid metabolism to now include mitochondrial metabolism and cellular energy balance.

Dataset Information

Mating regulates growth, metabolism, and digestive efficiency in the female Drosophila midgut

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets