Results for “omics” — Page 2

DOE OSTI2026

Temporal multi-omic analysis uncovers sex-biased molecular programs underlying skeletal muscle adaptation to endurance training

Background. Exercise training is known to benefit health and reduce disease risk. While adaptations in skeletal muscles are fundamental to many of the health benefits of exercise training, the common and sex-specific molecular regulators that mediate these adaptations remain to be fully elucidated. Methods. To this end, we leveraged skeletal muscle multi-omics data generated by the Molecular Transducers of Physical Activity Consortium (MoTrPAC), where 6 month-old male and female rats endurance trained for 1, 2, 4, or 8 weeks. Our objective was to identify shared and sex-specific multi-omic molecular responses to endurance training in skeletal muscle, and relate them to phenotypic adaptations. Results. We identified largely sexually-conserved transcriptomic and proteomic enrichments in the gastrocnemius, which correlated with skeletal muscle responses from a published exercise study in humans. We uncovered sex-consistent post-translational modifications, including decreased oxidation of MYH2 and deacetylation of the ß-oxidation enzyme HADHA. Pathway enrichment analyses revealed sex-specific remodeling across the acetylome, redox proteome, and phosphoproteome; females decreased mitochondrial protein oxidation and increased mitochondrial cristae proteins, indicative of enhanced redox buffering and mitochondrial efficiency. Despite observed decreases in the oxidation of key mitochondrial proteins, females displayed increases in the oxidation of proteins involved in glucose catabolism relative to males after 8 weeks of training, suggestive of sex-biased subcellular reactive oxygen species generation. Conclusions. This work shows a large portion of the adaptive response to endurance training in skeletal muscle is shared between females and males, while there are distinct and nuanced sex-specific adaptations that are evident, particularly at the level of post-translational regulation.

Many, Gina M.↗

DOE OSTI2025

A multi-omic characterization of the physiological responses to salt stress in Scenedesmus obliquus UTEX393

Scenedesmus obliquus UTEX393 is a promising microalgal candidate for sustainable biomanufacturing but its limited halotolerance hinders large-scale cultivation in saline environments. To investigate the molecular basis of salt stress responses, we conducted a comprehensive multi-omic analysis integrating genomics, transcriptomics, proteomics, lipidomics, metabolomics, and DNA affinity purification sequencing (DAP-seq). An improved nuclear genome assembly and annotation yielded 19,017 gene models and a 97% BUSCO completeness score, enabling construction of a genome-scale metabolic model. Comparing 15 ppt salinity stress to 5 ppt control, growth and productivity were significantly reduced, accompanied by widespread transcriptomic and proteomic changes. Transcriptomic analysis revealed downregulation of photosynthetic machinery and energy conservation genes, and upregulation of stress-responsive elements such as expansins, flavodoxins, and osmoprotectants. Lipidomic profiling showed accumulation of triacylglycerols (TAGs) and degradation of galactosyl lipids, consistent with a shift toward lipid biosynthesis to mitigate redox imbalance. Depletion of key polar metabolites and branched-chain amino acids suggested a rerouting of central carbon metabolism under stress. DAP-seq identified key transcription factors, including LHY1 and SPL12, that target central metabolic enzymes involved in redox balancing, such as glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and malate dehydrogenase (MDH). These findings establish a regulatory-metabolic framework linking redox stress to lipid accumulation and reveal potential engineering targets to enhance salt tolerance. Overall, the multi-omic analysis supports the “overflow” hypothesis, where impaired photosynthesis results in excess reducing equivalents being diverted into TAG synthesis and highlights transcriptional regulators as candidates for improving algal robustness in brackish environments.

09 BIOMASS FUELS↗

DOE OSTI2025

Holo-Omics disentangle drought response and biotic interactions among plant, endophyte and pathogen

Holo-omics provide a novel opportunity to study the interactions among fungi from different functional guilds in host plants in field conditions. We address the entangled responses of plant pathogenic and endophytic fungi associated with sorghum when droughted through the assembly of the most abundant fungal, endophyte genome from rhizospheric metagenomic sequences followed by a comparison of its metatranscriptome with the host plant metabolome and transcriptome. The rise in relative abundance of endophytic Acremonium persicinum (operational taxonomic unit 5 (OTU5)) in drought co-occurs with a rise in fungal membrane dynamics and plant metabolites, led by ethanolamine, a key phospholipid membrane component. The negative association between endophytic A. persicinum (OTU5) and plant pathogenic fungi co-occurs with a rise in expression of the endophyte's biosynthetic gene clusters coding for secondary compounds. Endophytic A. persicinum (OTU5) and plant pathogenic fungi are negatively associated under preflowering drought but not under postflowering drought, likely a consequence of variation in fungal fitness responses to changes in the availability of water and niche space caused by plant maturation over the growing season. Our findings suggest that the dynamic biotic interactions among host, beneficial and harmful microbiota in a changing environment can be disentangled by a blending of field observation, laboratory validation, holo-omics and ecological modelling.

Chen, Peilin↗

DOE OSTI2025

Multi-omics data compendium of pancreatic islet and β cell responses to pro-inflammatory cytokines

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 10 (Pck010)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 11 (Pck011)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 12 (Pck012)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 13 (Pck013)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 14 (Pck014)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 15 (Pck015)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 16 (Pck016)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 17 (Pck017)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 18 (Pck018)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 19 (Pck019)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 1 (Pck001)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 20 (Pck020)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 21 (Pck021)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗

DOE OSTI2025

Multi-omics data compendium: Data package 2 (Pck002)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗