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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. 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Biao Liu

PROVIDER: E-GEOD-45900 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2013-04-10 | GSE45900 | GEO

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

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

Transcription profiling of human pheochromocytomas of various genetic origins

Project description:Pheochromocytomas are neural crest-derived tumors that arise from inherited or sporadic mutations in at least six independent genes: RET, VHL, NF1, and subunits B, C and D of succinate dehydrogenase (SDH). The proteins encoded by these multiple genes regulate distinct functions. To identify molecular interactions between the distinct pathways we performed expression profiling of a large cohort of pheochromocytomas. We show here a functional link between tumors with VHL mutations and those with disruption of the genes encoding for succinate dehydrogenase (SDH) subunits B (SDHB) and D (SDHD). A transcription profile of reduced oxidoreductase is detected in all three of these tumor types, together with an angiogenesis/hypoxia profile typical of VHL dysfunction. The oxidoreductase defect, not previously detected in VHL-null tumors, is explained by suppression of the SDHB protein, a component of mitochondrial complex II. The decrease in SDHB is also noted in tumors with SDHD mutations. Gain-of-function and loss-of-function analyses show that the link between hypoxia signals (via VHL) and mitochondrial signals (via SDH) is mediated by HIF1?. These findings explain the shared features of pheochromocytomas with VHL and SDH mutations and suggest an additional mechanism for increased HIF1? activity in tumors.

2007-06-21 | E-GEOD-2841 | biostudies-arrayexpress

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

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

Expression Profiling of pheochromocytomas of various genetic origins

2005-08-12 | GSE2841 | GEO

Expression data from SDH-disabled GIST

Project description:Pediatric GIST commonly harbors a disabled succinate dehydrogenase complex (SDH), which yields tumors with highly conserved genomes but characteristic epigenomic signatures. Mysteriously, nearly half of such SDH-deficient GIST, including tumors from Carney Triad patients, lack identifiable mutations in SDH component genes and genes required for complex assembly (SDHA, SDHB, SDHC, SDHD, SDHAF, termed SDHx). Genomic sequencing coupled with DNA methylation and transcriptional profiling have exposed SDHC promoter-specific CpG island epimutation and concomitant gene silencing in the majority of SDHx-WT GIST.

2015-01-02 | GSE56670 | GEO

RNA seq of mouse CD3 T cells

Project description:Purpose: To gain more mechanistic insights into the effects of SDHB deletion in T cells, we performed RNAseq in activated WT and SDHB cKO T cells. Methods: Total RNA was isolated according to the RNeasy Mini Kit (Qiagen) and treated with DNase I. RNA quality was assessed using the Agilent 2100 Bioanalyzer and RNA Nano Chip kit (Agilent Technologies, CA). Results: RNA-seq revealed an enriched pro-inflammatory gene signature in SDHB cKO T cells after activation Conclusions: SDH inactivation results in a pro-inflammatory gene signature in T cells after activation

2022-03-08 | GSE184010 | GEO

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

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