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Multi-omics Analysis Unveils Metabolic Inflexibility Manifesting as Impaired Branched Amino Acid and Enhanced Fatty Acid Degradation in a Mouse Model of Diabetic Cardiomyopathy [ATAC-seq]

ABSTRACT: Multi-omics Analysis Unveils Metabolic Inflexibility Manifesting as Impaired Branched Amino Acid and Enhanced Fatty Acid Degradation in a Mouse Model of Diabetic Cardiomyopathy [ATAC-seq]

PROVIDER: PRJNA1146748 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30199679_1.fastq.gz	Fastqsanger.gz
	SRR30199679_2.fastq.gz	Fastqsanger.gz
	SRR30199680_1.fastq.gz	Fastqsanger.gz
	SRR30199680_2.fastq.gz	Fastqsanger.gz
	SRR30199681_1.fastq.gz	Fastqsanger.gz

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Multi-omics Analysis Unveils Metabolic Inflexibility Manifesting as Impaired Branched Amino Acid and Enhanced Fatty Acid Degradation in a Mouse Model of Diabetic Cardiomyopathy [RNA-seq]

Project description:Multi-omics Analysis Unveils Metabolic Inflexibility Manifesting as Impaired Branched Amino Acid and Enhanced Fatty Acid Degradation in a Mouse Model of Diabetic Cardiomyopathy [RNA-seq]

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Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

Project description:Branched‐chain amino acid (BCAA) metabolism is a central hub for energy production and regulation of numerous physiological processes. Controversially, both increased and decreased levels of BCAAs are associated with longevity. Using genetics and multi‐omics analyses in Caenorhabditis elegans, we identified adaptive regulation of the ubiquitin‐proteasome system (UPS) in response to defective BCAA catabolic reactions after the initial transamination step. Worms with impaired BCAA metabolism show a slower turnover of a GFP‐based proteasome substrate, which is suppressed by loss‐of‐function of the first BCAA catabolic enzyme, the branched‐chain aminotransferase BCAT‐1. The exogenous supply of BCAA‐derived carboxylic acids, which are known to accumulate in the body fluid of patients with BCAA metabolic disorders, is sufficient to regulate the UPS. The link between BCAA intermediates and UPS function presented here sheds light on the unexplained role of BCAAs in the aging process and opens future possibilities for therapeutic interventions.

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Nervous system reduction in branched-chain amino acid metabolism disrupts hippocampal neurogenesis and memory

Project description:To study the role of branched-chain amino acid metabolism in neural stem cells we generated two primary neural stem cell culture lines in which on was deleted for the Ppm1k gene using floxed cells and adenovirus delviered cre-recombinase.

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Drosophila miR-277 controls branched-chain amino acid catabolism and affects lifespan

Project description:Development, growth and adult survival are coordinated with available metabolic resources. The insulin/IGF and TOR signaling pathways relay nutritional status, thereby ascertaining that the organism responds appropriately to environmental conditions. MicroRNAs are short (21-23 nt) regulatory RNAs that confer specificity on the RNA-induced silencing complex (RISC) to inhibit a given set of mRNA targets. We profiled changes in miRNA expression during adult life in Drosophila melanogaster and determined that miR-277 is down-regulated with age. This miRNA controls branched-chain amino acid (BCAA) catabolism and the activity of the TOR kinase, a central growth regulator. Metabolite analysis suggests that the mechanistic basis may be an accumulation of BCKAs, rather than BCAAs, thus avoiding potentially detrimental consequences of increased branched chain amino acid levels on e.g. translational fidelity. Constitutive miR-277 expression as well as transgenic inhibition with a miRNA sponge construct shortens lifespan. Furthermore, constitutive miR-277 expression is synthetically lethal with reduced insulin signaling. Thus, optimal metabolic adaptation requires tuning of cellular BCAA catabolism by miR-277 to be concordant with systemic growth signaling.

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Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

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Reprograming of Proteasomal Degradation by Branched Chain Amino Acid Metabolism

Project description:Branched chain amino acids (BCAAs) play an important role in energy and protein regulation. Defects in BCAA metabolism are linked to numerous pathologies, including diabetes, neurodegeneration, and premature aging. Isovaleric acidemia is a metabolic disease caused by defective leucine breakdown and an abnormal accumulation of isovaleric acid in the body fluids; however, the cytotoxic effects caused by excess isovaleric acid remained unclear. Here, we provide a regulatory connection between BCAA metabolism and the ubiquitin/proteasome-system (UPS) in Caenorhabditis elegans. Multi-omic analysis identified that worms lacking the isovaleryl-CoA dehydrogenase IVD-1 exhibit reduced expression of regulatory proteasome subunits and defects in ubiquitin-dependent proteolysis. Conversely, proteasomal protein degradation was supported by the branched chain amino transferase BCAT-1. Adding extra isovaleric acid to the growth medium triggered UPS defects, implying a causative role of perturbed proteostasis in isovaleric academia.

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Multi-omics Analysis Unveils Metabolic Inflexibility Manifesting as Impaired Branched Amino Acid and Enhanced Fatty Acid Degradation in a Mouse Model of Diabetic Cardiomyopathy [RNA-seq]

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Multi-omics Analysis Unveils Metabolic Inflexibility Manifesting as Impaired Branched Amino Acid and Enhanced Fatty Acid Degradation in a Mouse Model of Diabetic Cardiomyopathy [ATAC-seq]

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Branched chain amino acid sufficiency is necessary for proper luteinizing hormone response, testosterone synthesis, and motor coordination

Project description:Loss of branched-chain α-keto acid dehydrogenase kinase (BCKDK) increases branched-chain amino acid (BCAA) oxidation by disinhibiting BCKDH. We previously observed that in Bckdk knockout (KO) mice circulating BCAA levels are significantly reduced, negatively affecting neurological function, motor behavior, and male fertility. This work comparatively assessed how systemic loss of Bckdk modulates the transcriptome in testes and skeletal muscle under control diet feeding. Freely-fed adult male C57BL6/J mice and Bckdk KO mice on the C57BL6/J genetic background were euthanized by decapitation at the mid-point of the light cycle and tissues were quickly harvested and frozen in liquid nitrogen. Total RNA was extracted from frozen testes and hind-limb muscle (gastrocnemius and plantaris combined).

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