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Characterizing gene expression changes that accompany succinate dehydrogenase subunit B (SDHB) RNA editing in monocyte-enriched peripheral blood mononuclear cell cultures

ABSTRACT: The goal of this study is to identify global changes in gene expression that accompany induction of site-specific RNA editing that targets the SDHB gene in monocyte-enriched peripheral blood mononuclear cell cultures. The results provide important information to understand the function of this programmed SDHB RNA mutation within the context of global gene expression changes that occur in cultured immune cells when the editing is induced. The study also specifically tests whether expression changes occur in SDH subunit genes, cytidine deaminase family of genes and hypoxia-inducible pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45900 | GEO | 2013/04/10

SECONDARY ACCESSION(S): PRJNA196620

REPOSITORIES: GEO

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Characterizing gene expression changes that accompany succinate dehydrogenase subunit B (SDHB) RNA editing in monocyte-enriched peripheral blood mononuclear cell cultures

Project description:The goal of this study is to identify global changes in gene expression that accompany induction of site-specific RNA editing that targets the SDHB gene in monocyte-enriched peripheral blood mononuclear cell cultures. The results provide important information to understand the function of this programmed SDHB RNA mutation within the context of global gene expression changes that occur in cultured immune cells when the editing is induced. The study also specifically tests whether expression changes occur in SDH subunit genes, cytidine deaminase family of genes and hypoxia-inducible pathways. Overall design includes pairwise comparison of total gene expression profiles from uncultured cold-aggregated PBMCs (day 0), low-editing (culture day 3) and high-editing (culture days 5-8) samples, each from 4 donors. Submitted manuscript reported summary results from comparison of cultured low- and high-editing samples.

2013-04-10 | E-GEOD-45900 | biostudies-arrayexpress

Immunoprecipitation of Toxoplasma gondii succinate dehydrogenase complex

Project description:The apicomplexan parasite Toxoplasma gondii has a divergent mitochondrial electron transport chain (mETC). Succinate dehydrogenase (SDH), the second complex in the mETC and an enzyme in the TCA cycle, has 4 subunits in common model organisms, but Toxoplasma has a 9 subunit SDH complex. We performed immunoprecipitation of SDH, via an HA epitope tagged SDHB subunit, and the unrelated Complex III and analysed the elution via LFQ mass spectrometry, to confirm the composition of the divergent Toxoplasma gondii SDH complex.

2023-12-27 | PXD047027 | Pride

The SDHB Arg230His mutation causing familial paraganglioma alters glycolysis in a new Caenorhabditis elegans model

Project description:The conserved B-subunit of succinate dehydrogenase (SDH) participates in the TCA cycle and mitochondrial electron transport. The Arg230His mutation in SDHB causes heritable pheochromocytoma/paraganglioma (PPGL). In C. elegans, we generated an in vivo PPGL model (SDHB-1 Arg244His; equivalent to human Arg230His) which manifests delayed development, shortened lifespan, attenuated ATP production and reduced mitochondrial number. Although succinate is elevated in both missense and null sdhb-1(gk165) mutants, transcriptomic comparison suggests very different causal mechanisms that are supported by metabolic analysis where only Arg244His (not null) worms elevate lactate/pyruvate levels, pointing to a missense-induced, ‘Warburg’-like aberrant glycolysis. In silico predictions of the SDHA-B dimer structure demonstrate that Arg230His modifies the catalytic cleft despite the latter’s remoteness from the mutation site. We hypothesise that Arg230His SDHB mutation rewires metabolism, reminiscent of metabolic reprogramming in cancer. Our tractable model provides a novel tool to investigate the metastatic propensity of this familial cancer and our approach may illuminate wider SDH pathology.

2020-10-01 | GSE158836 | GEO

Gene expression profiling of mouse cells deficient for succinate dehydrogenase

Project description:Pheochromocytoma (PCC) and paraganglioma (PGL) are neuroendocrine tumours arising in the adrenal medulla and paraganglia of the autonomous nervous system, respectively. Malignant PCC/PGL are mostly caused by germline mutations of SDHB, encoding a subunit of succinate dehydrogenase. Gene expression changes associated with SDHB inactivation were investigated in a two genetically defined murine cellular models. These models were generated by Cre-mediated recombination in spontaneously immortalized mouse chromaffin cells (imCCs) and adrenal fibroblasts (MAFs).

2015-11-04 | E-MTAB-3403 | biostudies-arrayexpress

Transcription profiling of S. cerevisiae following the deletion of succinate dehydrogenase

Project description:Background; Mitochondrial respiration is an important and widely conserved cellular function in eukaryotic cells. The succinate dehydrogenase complex (SDH-complex) plays an important role in respiration as it connects the mitochondrial respiratory chain to the tricarboxylic acid (TCA) cycle where it catalyzes the oxidation of succinate to fumarate. Cellular response to the SDH-complex dysfunction (i.e. impaired respiration) thus has important implications not only for biotechnological applications but also for understanding cellular physiology underlying metabolic diseases such as diabetes. We therefore explored the physiological and transcriptional response of Saccharomyces cerevisiae to the deletion of SDH3, that codes for an essential subunit of the SDH-complex. Results; Although the SDH-complex has no direct role in transcriptional regulation and the flux through the corresponding reaction under the studied conditions is very low, deletion of SDH3 resulted in significant changes in the expression of several genes involved in various cellular processes ranging from metabolism to the cell-cycle. By using various bioinformatics tools we explored the organization of these transcriptional changes in the metabolic and other cellular functional interaction networks. Conclusions; Our results show that the transcriptional regulatory response resulting from the impaired respiratory function is linked to several different parts of the metabolism, including fatty acid and sterol metabolism. Experiment Overall Design: Two replicates for sdh3 deletion mutants. Reference strain transcriptome data: Westergaard SL et al., FEMS Yeast Res 2004, 5: 193-204.

2009-01-13 | E-GEOD-13924 | biostudies-arrayexpress

Global transcriptional response of Saccharomyces cerevisiae following the deletion of succinate dehydrogenase

Project description:Background Mitochondrial respiration is an important and widely conserved cellular function in eukaryotic cells. The succinate dehydrogenase complex (SDH-complex) plays an important role in respiration as it connects the mitochondrial respiratory chain to the tricarboxylic acid (TCA) cycle where it catalyzes the oxidation of succinate to fumarate. Cellular response to the SDH-complex dysfunction (i.e. impaired respiration) thus has important implications not only for biotechnological applications but also for understanding cellular physiology underlying metabolic diseases such as diabetes. We therefore explored the physiological and transcriptional response of Saccharomyces cerevisiae to the deletion of SDH3, that codes for an essential subunit of the SDH-complex. Results Although the SDH-complex has no direct role in transcriptional regulation and the flux through the corresponding reaction under the studied conditions is very low, deletion of SDH3 resulted in significant changes in the expression of several genes involved in various cellular processes ranging from metabolism to the cell-cycle. By using various bioinformatics tools we explored the organization of these transcriptional changes in the metabolic and other cellular functional interaction networks. Conclusions Our results show that the transcriptional regulatory response resulting from the impaired respiratory function is linked to several different parts of the metabolism, including fatty acid and sterol metabolism.

2008-12-16 | GSE13924 | GEO

Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

Project description:Drug resistance is vital for the poor prognosis of acute myeloid leukemia (AML) patients, but the underlying mechanism remains poorly understood. Given the unique microenvironment of bone marrow, we reasoned that drug resistance of AML might rely on distinct microenvironment-associated metabolic processes. Here, we identified SDH deficiency and over-cumulative succinate as typical features in AML, with a marked function in causing the resistance of AML cells to a wide range of anti-cancer therapies. Mechanistically, succinate promoted the accumulation of oncogenic proteins in a manner that precedes transcriptional activation. This function was mediated by succinate-triggered upregulation of UBC12 phosphorylation, which impaired its E2 function in cullins neddylation. Notably, decreasing succinate levels by fludarabine could effectively restore the drug sensitivity of SDH-deficient AML PDX. Together, we uncover a novel function of succinate in driving drug resistance by regulating p-UBC12/cullin activity, and indicate reshaping succinate metabolism as a promising treatment for SDH-deficient AML.

2024-08-27 | GSE247623 | GEO

Succinate dehydrogenase (SDH)-Complex II regulates skeletal muscle cellular respiration and fatigue but not muscle mass in genetically induced pulmonary emphysema [20 wk]

Project description:Skeletal muscle wasting and reduced oxidative capacity coexist in patients with COPD/pulmonary emphysema and are independently associated with higher mortality. Whether reduced respiration contributes to muscle atrophy in that setting remains unknown. We have previously shown that a mouse with genetically induced COPD/pulmonary emphysema recapitulates muscle dysfunction features present in patients’ muscles, including reduced expression and activity of succinate dehydrogenase (SDH), which are partially reversed by genetic gain of SDH function. Previous research suggests that succinate accumulation, a by-product of SDH inhibition, can increase respiratory capacity of skeletal muscle. Here, we generated an inducible, muscle-specific SDH-C knockout mouse which demonstrates lower mitochondrial oxygen consumption and oxidative fibers’ contractility, associated with overall reduced exercise endurance. These changes are partially offset by mitochondrial complex I-dependent respiration, a respiratory pattern replicated in the muscles from the COPD/pulmonary emphysema genetic model. Moreover, while mice skeletal muscle SDH-C knockout causes an early succinate accumulation associated with a downregulated transcriptome, these changes do not correlate with the proteomic landscape; and animals muscle mass, fiber-type composition, and dry body mass constituents remain unaltered. We preset the first conditional, skeletal muscle-specific SDH-C knockout animal and demonstrate that while SDH-C regulates fibers respiration in genetically induced pulmonary emphysema, it does not control muscle mass.

2024-02-24 | GSE255635 | GEO

Succinate dehydrogenase (SDH)-Complex II regulates skeletal muscle cellular respiration and fatigue but not muscle mass in genetically induced pulmonary emphysema [3 wk]

2024-02-24 | GSE255632 | GEO

Gene expression analysis of SDH-deficient immortalized kidney epithelial cells

Project description:Succinate dehydrogenase (SDH) is a mitochondrial protein complex responsible for the oxidation of succinate to fumarate in the tricarboxylic acid cycle. Loss-of-function mutations in any of the SDH genes are associated with susceptibility to develop neu-roendrocrine neoplasms and renal cell carcinoma. However, the impact of SDH loss on cell metabolism and the mechanisms enabling growth of SDH-defective cells are largely unexplored. To address this issue we generated Sdhb-ablated kidney mouse cells and compared their transcriptomic profile with that of Sdhb-proficient cells. Results of this gene analysis are provided in the here deposited gene array.

2016-01-22 | E-MTAB-4349 | biostudies-arrayexpress

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