Cold adaptation shapes the robustness of metabolic networks in Drosophila melanogaster
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila Melanogaster
TISSUE(S): Whole Insect
PROVIDER: ST000102 | MetabolomicsWorkbench |
REPOSITORIES: MetabolomicsWorkbench
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| mwtab | Other |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:When ectotherms are exposed to low temperatures, they enter a cold-induced coma (chill coma) that prevents resource acquisition, mating, oviposition, and escape from predation. There is substantial variation in time taken to recover from chill coma both within and among species, and this variation is correlated with habitat temperatures such that insects from cold environments recover more quickly. This suggests an adaptive response, but the mechanisms underlying variation in recovery times are unknown, making it difficult to decisively test adaptive hypotheses. We use replicated lines of Drosophila melanogaster selected in the laboratory for fast (hardy) or slow (susceptible) chill-coma recovery times to investigate modifications to metabolic profiles associated with cold adaptation. We measured metabolite concentrations of flies before, during, and after cold exposure using nuclear magnetic resonance (NMR) spectroscopy to test the hypotheses that hardy flies maintain metabolic homeostasis better during cold exposure and recovery, and that their metabolic networks are more robust to cold-induced perturbations. The metabolites of cold-hardy flies were less cold responsive and their metabolic networks during cold exposure were more robust, supporting our hypotheses. Metabolites involved in membrane lipid synthesis, tryptophan metabolism, oxidative stress, energy balance, and proline metabolism were altered by selection on cold tolerance. We discuss the potential significance of these alterations.
| S-EPMC4472466 | biostudies-literature
Project description: Not available
| ST000101 | MetabolomicsWorkbench
Project description:Competition for substrates is a ubiquitous selection pressure faced by microbes, yet intracellular trade-offs can prevent cells from metabolizing every type of available substrate. Adaptive evolution is constrained by these trade-offs, but their consequences for the repeatability and predictability of evolution are unclear. Here we develop an eco-evolutionary model with a metabolic trade-off to generate networks of mutational paths in microbial communities and show that these networks have descriptive and predictive information about the evolution of microbial communities. We find that long-term outcomes, including community collapse, diversity, and cycling, have characteristic evolutionary dynamics that determine the entropy, or repeatability, of mutational paths. Although reliable prediction of evolutionary outcomes from environmental conditions is difficult, graph-theoretic properties of the mutational networks enable accurate prediction even from incomplete observations. In conclusion, we present a novel methodology for analyzing adaptive evolution and report that the dynamics of adaptation are a key variable for predictive success.The structure and dynamics of microbial communities reflect trade-offs in the ability to use different resources. Here, Josephides and Swain incorporate metabolic trade-offs into an eco-evolutionary model to predict networks of mutational paths and the evolutionary outcomes for microbial communities.
| S-EPMC5612958 | biostudies-literature
Project description:The gut microbiota plays a key role in host metabolic thermogenesis by activating UCP1 and increasing the browning process of white adipose tissue (WAT), especially in cold environments. However, the crosstalk between the gut microbiota and the host, which lacks functional UCP1, making them susceptible to cold stress, has rarely been illustrated. We used male piglets as a model to evaluate the host response to cold stress via the gut microbiota (four groups: room temperature group, n = 5; cold stress group, n = 5; cold stress group with antibiotics, n = 5; room temperature group with antibiotics, n = 3). We found that host thermogenesis and insulin resistance increased the levels of serum metabolites such as glycocholic acid (GCA) and glycochenodeoxycholate acid (GCDCA) and altered the compositions and functions of the cecal microbiota under cold stress. The gut microbiota was characterized by increased levels of Ruminococcaceae, Prevotellaceae, and Muribaculaceae under cold stress. We found that piglets subjected to cold stress had increased expression of genes related to bile acid and short-chain fatty acid (SCFA) metabolism in their liver and fat lipolysis genes in their fat. In addition, the fat lipolysis genes CLPS, PNLIPRP1, CPT1B, and UCP3 were significantly increased in the fat of piglets under cold stress. However, the use of antibiotics showed a weakened or strengthened cold tolerance phenotype, indicating that the gut microbiota plays important role in host thermogenesis. Our results demonstrate that the gut microbiota-blood-liver and fat axis may regulate thermogenesis during cold acclimation in piglets.
| S-EPMC8983680 | biostudies-literature
Project description:Metabolic flexibility is an important component of adaptation to stressful environments, including thermal stress and latitudinal adaptation. A long history of population genetic studies suggest that selection on core metabolic enzymes may shape life histories by altering metabolic flux. However, the direct relationship between selection on thermal stress hardiness and metabolic flux has not previously been tested. We investigated flexibility of nutrient catabolism during cold stress in Drosophila melanogaster artificially selected for fast or slow recovery from chill coma (i.e. cold-hardy or -susceptible), specifically testing the hypothesis that stress adaptation increases metabolic turnover. Using (13)C-labelled glucose, we first showed that cold-hardy flies more rapidly incorporate ingested carbon into amino acids and newly synthesized glucose, permitting rapid synthesis of proline, a compound shown elsewhere to improve survival of cold stress. Second, using glucose and leucine tracers we showed that cold-hardy flies had higher oxidation rates than cold-susceptible flies before cold exposure, similar oxidation rates during cold exposure, and returned to higher oxidation rates during recovery. Additionally, cold-hardy flies transferred compounds among body pools more rapidly during cold exposure and recovery. Increased metabolic turnover may allow cold-adapted flies to better prepare for, resist and repair/tolerate cold damage. This work illustrates for the first time differences in nutrient fluxes associated with cold adaptation, suggesting that metabolic costs associated with cold hardiness could invoke resource-based trade-offs that shape life histories.
| S-EPMC5031658 | biostudies-literature
Project description: Not available
| ST000097 | MetabolomicsWorkbench
Project description:In response to cold, brown adipose tissue (BAT) increases its metabolic rate and expands its mass to produce heat required for survival, a process known as BAT recruitment. The mechanistic target of rapamycin complex 1 (mTORC1) controls metabolism, cell growth and proliferation, but its role in regulating BAT recruitment in response to chronic cold stimulation is unknown. Here, we show that cold activates mTORC1 in BAT, an effect that depends on the sympathetic nervous system. Adipocyte-specific mTORC1 loss in mice completely blocks cold-induced BAT expansion and severely impairs mitochondrial biogenesis. Accordingly, mTORC1 loss reduces oxygen consumption and causes a severe defect in BAT oxidative metabolism upon cold exposure. Using in vivo metabolic imaging, metabolomics and transcriptomics, we show that mTORC1 deletion impairs glucose and lipid oxidation, an effect linked to a defect in tricarboxylic acid (TCA) cycle activity. These analyses also reveal a severe defect in nucleotide synthesis in the absence of mTORC1. Overall, these findings demonstrate an essential role for mTORC1 in the regulation of BAT recruitment and metabolism in response to cold.
| S-EPMC5120333 | biostudies-literature
Project description: Not available
| ST000099 | MetabolomicsWorkbench
Project description:We have determined the transcriptional response of the budding yeast Saccharomyces cerevisiae to cold. Yeast cells were exposed to 10 degrees C for different lengths of time, and DNA microarrays were used to characterize the changes in transcript abundance. Two distinct groups of transcriptionally modulated genes were identified and defined as the early cold response and the late cold response. A detailed comparison of the cold response with various environmental stress responses revealed a substantial overlap between environmental stress response genes and late cold response genes. In addition, the accumulation of the carbohydrate reserves trehalose and glycogen is induced during late cold response. These observations suggest that the environmental stress response (ESR) occurs during the late cold response. The transcriptional activators Msn2p and Msn4p are involved in the induction of genes common to many stress responses, and we show that they mediate the stress response pattern observed during the late cold response. In contrast, classical markers of the ESR were absent during the early cold response, and the transcriptional response of the early cold response genes was Msn2p/Msn4p independent. This implies that the cold-specific early response is mediated by a different and as yet uncharacterized regulatory mechanism.
| S-EPMC532028 | biostudies-literature
Project description:Cold environments dominate Earth's biosphere, hosting complex microbial communities with the ability to thrive at low temperatures. However, the underlying molecular mechanisms and the metabolic pathways involved in bacterial cold-adaptation mechanisms are still not fully understood. Herein, we assessed the metabolic features of the Antarctic bacterium Pseudoalteromonas haloplanktis TAC125 (PhTAC125), a model organism for cold-adaptation, at both 4 °C and 15 °C, by integrating genomic and phenomic (high-throughput phenotyping) data and comparing the obtained results to the taxonomically related Antarctic bacterium Pseudoalteromonas sp. TB41 (PspTB41). Although the genome size of PspTB41 is considerably larger than PhTAC125, the higher number of genes did not reflect any higher metabolic versatility at 4 °C as compared to PhTAC125. Remarkably, protein S-thiolation regulated by glutathione and glutathionylspermidine appeared to be a new possible mechanism for cold adaptation in PhTAC125. More in general, this study represents an example of how 'multi-omic' information might potentially contribute in filling the gap between genotypic and phenotypic features related to cold-adaptation mechanisms in bacteria.
| S-EPMC5429795 | biostudies-literature