Search bioRxiv⌕ Search

bioRxiv · 10.1101/2020.06.07.139139

Different protein metabolic strategies for growth during food-induced physiological plasticity

Abstract

Food-induced morphological plasticity, a type of developmental plasticity, is a well-documented phenomenon in larvae of the echinoid echinoderm, Dendraster excentricus. A recent study in our lab has shown that this morphological plasticity is associated with significant physiological plasticity for growth. The goal of the current study was to measure several aspects of protein metabolism in larvae growing at different rates to understand the mechanistic basis for this physiological growth plasticity. Larvae of D. excentricus were fed rations of 1,000 (low-fed) or 10,000 (high-fed) algal cells mL−1. Primary measurements of protein growth, algal ingestion, aerobic metabolism, alanine transport and protein synthesis were used to model growth and protein metabolism. Relative protein growth rates were 6.0 and 12.2 % day−1 for low- and high-fed larvae, respectively. The energetic cost of protein synthesis was similar between both treatments at 4.91 J (mg protein synthesized)−1. Larvae in both treatments used about 50% of their metabolic energy production to fuel protein synthesis. Mass-specific rates of protein synthesis were also similar. The most important difference between low- and high-fed larvae were mass-specific rates of protein degradation. Low-fed larvae had relatively low rates of degradation early in development that increased with larval age, surpassing high-fed degradation rates at 20 days post-fertilization. Changes in protein depositional efficiency during development were similar to those of larval growth efficiency, indicating that differences in protein metabolism are largely responsible for whole-organism growth plasticity. Mass-specific alanine transport rates were about 2-times higher in low-fed larvae, demonstrating that the longer arms of low-fed larvae may be a mechanism for acquiring more dissolved nutrients from their environment. In total, these results provide an explanation for the differences in growth efficiency between low- and high-fed larvae and demonstrate the importance of protein degradation pathways in establishing these growth differences. These observations, together with previous studies measuring morphological and physiological plastic responses, allow for a more integrated understanding of developmental plasticity in echinoid larvae.AbbreviationsDPFdays post-fertilizationPOpostoral armAEassimilation efficiencyGGEgross growth efficiencyNGEnet growth efficiencyPGEprotein growth efficiencyPDEprotein depositional efficiencyMBLmidline body lengthFAAfree amino acid poolRGRrelative growth rateBCAbicinchoninic assayBSAbovine serum albuminTCAtrichloroacetic acidBODbiological oxygen demandTORtarget of rapamycinDOMdissolved organic materialView Full Text

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ellison, A., Pouv, A., Pace, D. A.. 2020-06-08. Different protein metabolic strategies for growth during food-induced physiological plasticity. https://doi.org/10.1101/2020.06.07.139139

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The canine hair metabolome encodes age and coat exposure in over 700 dogs

Hair can be collected noninvasively and stored for years, making it a practical sample for studying physiology and environmental exposure. Yet the chemical information it carries in dogs remains largely unexplored. We profiled 782 banked hair samples from 700 Golden Retrievers by untargeted liquid chromatography-mass spectrometry, detecting 4,533 compound groups and revealing an unexpectedly rich chemical profile. Prominent signals reflected skin-surface and hair chemistry, including amino acids, peptides and urocanic acid, alongside surfactants, plasticizers and pesticides detectable despite washing. A signal annotated as imidacloprid distinguished dogs receiving topical products containing this insecticide from dogs receiving no flea or tick preventive (AUC 0.865). Hair chemistry also varied with age, most strongly between puppyhood and early adulthood. Oxidized lipids generally declined, whereas amino acids and peptides remained largely stable. A multivariate model estimated age with moderate accuracy (cross-validated r = 0.66) and assigned a higher age to the later sample in 64 of 75 repeatedly sampled dogs. Because age and collection date were strongly correlated, their effects could not be fully separated, although date-restricted analyses supported an age-related contribution. Together, these findings establish banked dog hair as a promising resource for studying chemical exposure and life-stage-associated changes in chemistry.

physiology↗

Dietary Human HSP90 Promotes Longevity and Healthspan in Caenorhabditis elegans via a Multi-Branched Stress Signaling Pathway

The loss of proteostasis is one of the primary drivers of aging. Despite the important role of the molecular chaperone HSP90 in maintaining proteostasis, its systemic role in aging appears contradictory because its inhibitors can effectively extend lifespan across diverse species. This study showed that dietary HSP90 supplementation via Escherichia coli significantly extended lifespan and healthspan of Caenorhabditis elegans without fertility trade-offs. Exogenous HSP90 likely acts as an extracellular signaling ligand that engages downstream kinase networks to drive the activation of three major longevity-associated transcription factors: DAF-16, SKN-1, and HSF-1. In addition, we demonstrated the additive effect of combining dietary HSP90 supplementation with the senolytic HSP90 inhibitor tanespimycin, indicating that extracellular proteostatic signaling and the intracellular inhibition of HSP90 can work together to enhance longevity. Finally, we engineered an antibiotic-free E. coli Nissle 1917 probiotic that constitutively expresses HSP90, which successfully extended the lifespan of C. elegans.

physiology↗

Sex differences in myocardial ketone oxidation capacity in cardiometabolic disease with coincident ischemic heart disease

Background: Myocardial infarction (MI) in patients with heart failure with preserved ejection fraction (HFpEF) is associated with worse outcomes than MI in individuals without HFpEF. However, the molecular mechanisms underlying this increased vulnerability remain poorly understood. We investigated sex differences in cardiac ketone body (KB) metabolism in patients with diabetes-associated ischemic heart disease, and in a mouse model of HFpEF complicated by MI (HFpEF-MI). Methods: Cardiac BDH1 and OXCT1 expression was assessed in male and female patients with diabetes, with or without ischemic heart disease. Male and female mice received a high-fat diet and L-NAME for 10 weeks to induce HFpEF, followed by coronary artery ligation to induce MI. Glucose tolerance, cardiac function, survival, cardiac KB oxidative capacity, and circulating KB levels were evaluated. Results: Cardiac BDH1 and OXCT1 abundance was significantly reduced in male patients with diabetes-associated ischemic heart disease but preserved in female patients. In mice, 10 weeks of high-fat diet and L-NAME administration increased fasting blood glucose and impaired glucose tolerance. MI reduced systolic function in control and HFpEF mice of both sexes. Male HFpEF-MI mice exhibited higher mortality than female HFpEF-MI mice. Consistent with our human results, male HFpEF-MI mice showed reduced cardiac ketolytic enzyme expression alongside elevated circulating KB levels, whereas female mice maintained cardiac KB oxidative capacity. Conclusion: Reduced cardiac ketolytic enzyme expression and impaired KB oxidative capacity are associated with greater mortality in male HFpEF-MI mice, whereas female mice exhibit preserved KB oxidative capacity and improved survival. Similar sex differences in ketolytic enzyme expression were observed in patients with diabetes-associated ischemic heart disease. These findings identify cardiac ketone metabolism as a potential therapeutic target warranting further investigation in HFpEF complicated by MI.

physiology↗