bioRxiv Science⌕ Search

bioRxiv · 10.1101/2022.08.26.505340

Combined single-sample metabolomics and RNAseq reveals a hepatic pyrimidine metabolic response to acute viral infection

Abstract

ObjectiveMetabolomics and RNA sequencing (RNAseq) each provide powerful readouts of phenotype, and integration of these data can provide information greater than the sum of their parts. The ability to conduct such analysis on a single sample has many practical advantages, especially when dealing with rare or difficult-to-obtain samples. While methods exist to isolate multiple biomolecular subclasses from the same sample, in-depth analysis of the suitability of these approaches for multi- omics readouts is lacking. MethodsMice were injected with lymphocytic choriomeningitis virus (LCMV) or vehicle (Veh) control and liver tissue was harvested 2.5-days later. RNA was isolated from aliquots of pulverized liver tissue either following metabolite extraction using 80% methanol (MetRNA) or directly from frozen tissue (RNA). RNA sequencing data was evaluated by differential expression analysis via edgeR and dispersion using Ginis mean differences. Differential metabolite abundance was assessed using LIMMA. Pathway enrichment analysis was conducted on metabolomics and RNAseq data using MetaboAnalysts joint-integration tools. ResultsPrior metabolite extraction had no deleterious effects on quality or quantity of isolated RNA. RNA and MetRNA generated from the same sample clustered together by principal component analysis, indicating that inter-individual differences were the largest source of variance. Of the 2,169 genes that were differentially expressed between LCMV and Veh, the vast majority (n=1,848) were shared between extraction method, with the remainder evenly divided between RNA (n=165) and MetRNA (n=156). These differentially expressed genes unique to extraction method were attributed to randomness around the false discovery rate (FDR) = 0.05 cutoff and stochastic changes in variance estimation. Gini analysis further revealed that extraction method had no effect on the dispersion of detected transcripts across the entire dataset. To demonstrate the power of multi-omics integration on interrogated metabolic phenotypes, we next performed integrated pathway enrichment analysis on RNAseq data and metabolomics data. Our analysis revealed pyrimidine metabolism as the most impacted pathway by LCMV infection. Plotting up- and down-regulated genes and metabolites on the Kyoto Encyclopedia of Genes and Genomes (KEGG) pyrimidine pathway exposed a pattern enzymatic degradation of pyrimidine nucleotides to generate the nucleobase uracil. Further, uracil was among the most differentially abundant metabolite in serum of LCMV infected mice, suggesting a novel mechanism of hepatic uracil export in acute infection response. ConclusionsWe demonstrate that prior metabolite extraction does not have a deleterious effect on RNAseq quality, which enables investigators to confidently perform metabolomics and RNAseq on the same sample. Implementation of this approach revealed a novel involvement of the hepatic pyrimidine metabolism during acute viral infection.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Madaj, Z. B., Dahabieh, M. S., Kamalumpundi, V., Muhire, B., Pettinga, D. J., Siwicki, R. A., Ellis, A. E., Isaguirre, C., Escobar Galvis, M. L., DeCamp, L., Jones, R. G., Givan, S. A., Adams, M., Sheldon, R. D.. 2022-08-26. Combined single-sample metabolomics and RNAseq reveals a hepatic pyrimidine metabolic response to acute viral infection. https://doi.org/10.1101/2022.08.26.505340

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

KEEP EXPLORING

Related preprints

Trans-branching of polyubiquitin chains orchestrates the DNA replication stress response

Polyubiquitin chain geometry dictates functional consequences of ubiquitylation. Although branched polyubiquitin chains are abundant in cells, little is known about their functions. Here we show that branching on the DNA replication factor PCNA, mediated by the ubiquitin-conjugating enzyme UBE2K and involving lysines 63 and 48 of ubiquitin, orchestrates the sequence of events in response to replication stress. By inducing VCP-dependent extraction of PCNA from chromatin, branching promotes re-priming of stalled forks and necessitates a BRCA1-dependent pathway of daughter-strand gap repair. Our study identifies hyper-accumulation of daughter-strand gaps as the mechanistic basis underlying the toxicity of inhibitors of the PCNA-specific isopeptidase, USP1, in BRCA1-deficient cells. Moreover, an unexpected preference of UBE2K to operate in trans suggests a general timing mechanism to organize hierarchies amongst ubiquitin signals.

molecular biology↗

Impaired proteostasis is an early feature of the diabetic heart in humans and mice

Diabetes and obesity increase cardiac lipid levels leading to cardiomyopathy and heart failure. We hypothesized that intermittent fasting would reduce cardiac lipid levels. Surprisingly, intermittent fasting increased myocardial triglyceride content, but rescued mortality and attenuated cardiomyopathy in mice overexpressing cardiomyocyte acyl-CoA synthetase 1 (MHC-ACSL1). Lipid overload caused cardiomyocyte accumulation of polyubiquitinated protein aggregates containing desmin, a scaffolding intermediate filament protein, which intermittent fasting prevented. Furthermore, intermittent fasting reversed elevated myocardial C16:0 ceramide content, and knockdown of ceramide synthase CerS5 and CerS6 reduced palmitate-induced protein aggregation, highlighting a role for C16:0 ceramides in this pathology. Conversely, impairing aggrephagy with cardiomyocyte-specific p62 ablation induced heart failure in mice fed a high-fat diet, with paradoxically reduced cardiac lipid content. Crucially, non-failing diabetic human hearts also exhibited protein aggregate pathology. Taken together, these results demonstrate that impaired proteostasis characterizes cardiomyopathy from cardiac lipid overload and identify a promising new therapeutic target for this condition.

molecular biology↗

Spatial profiling and neurovascular communication in the developing and adolescent cortex following prenatal alcohol exposure

Fetal alcohol spectrum disorders (FASD) constitute a wide range of developmental, cognitive, and behavioral impairments caused by prenatal alcohol exposure (PAE). Although neuronal and vascular consequences of PAE have been studied, how alcohol affects the cerebrovasculature within the framework of the neurovascular unit (NVU) across development remains poorly understood. At minimum, the NVU comprises neurons, astrocyte endfeet, and endothelial cells (ECs), which coordinate to maintain brain homeostasis. Here, we used the NanoString Digital Spatial Profiling platform to characterize spatial transcriptomic data from neurons, astrocytes, and ECs from PAE and saccharin (SAC) control cortices at embryonic day 18 (E18) and postnatal day 28 (P28). Differentially expressed genes were then used for Ingenuity Pathway Analysis (IPA) to identify altered biological pathways and perform comparison analyses across developmental time points, while CellChat was used to infer cell cell communication networks. We uncovered thousands of differentially expressed genes and numerous altered pathways and biological processes in PAE cortices across development. Both IPA and CellChat analyses implicated dysregulation of vascular and extracellular matrix (ECM) remodeling, cell adhesion, and neuroinflammatory signaling. CellChat further predicted the loss of several key bidirectional relationships and altered ligand-receptor interactions among neurovascular cell types at E18 and P28. Overall, these findings identify PAE associated alterations in neurovascular gene expression and intercellular signaling across development, providing potential mechanisms by which PAE may disrupt neurodevelopment.

molecular biology↗