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RNA-seq Files : The Hypoxia Response Pathway Promotes PEP Carboxykinase And Gluconeogenesis In C. elegans

ABSTRACT: RNA was isolated from L4 stage animals for the following genotypes: N2, hif-1(ia4), egl-9(sa307), hif-1(ia4);egl-9(sa307) grown at 20C. Total RNA was isolated and used to prepare libraries using the Illumina Truseq with polyA selection. Libraries were sequenced across two lanes on an Illumina HiSeq2000 (GeneWiz) or an Illumina HiSeq 2500 in Rapid Run Mode (RUCDR).

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE173580 | GEO | 2022/09/19

REPOSITORIES: GEO

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ChIP-Seq Files : The Hypoxia Response Pathway Promotes PEP Carboxykinase And Gluconeogenesis In C. elegans

Project description:To identify genes directly regulated by HIF-1, we performed ChIP-seq on L4-stage egl-9(sa307); hif-1(ia4); odIs131[hif-1::gfp] animals, which have activated HIF-1 under aerobic conditions, using anti-GFP antibodies to precipitate DNA bound by HIF-1::GFP followed by high-throughput sequencing to identify peaks of reads corresponding to HIF-1 binding sites

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The Hypoxia Response Pathway Promotes PEP Carboxykinase And Gluconeogenesis In C. elegans

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-19 | GSE173581 | GEO

Phylogenetic study of the evolution of PEP-carboxykinase.

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Phosphoenolpyruvate carboxykinase in cell metabolism: Roles and mechanisms beyond gluconeogenesis.

Project description:BackgroundPhosphoenolpyruvate carboxykinase (PCK) has been almost exclusively recognized as a critical enzyme in gluconeogenesis, especially in the liver and kidney. Accumulating evidence has shown that the enhanced activity of PCK leads to increased glucose output and exacerbation of diabetes, whereas the defects of PCK result in lethal hypoglycemia. Genetic mutations or polymorphisms are reported to be related to the onset and progression of diabetes in humans.Scope of reviewRecent studies revealed that the PCK pathway is more complex than just gluconeogenesis, depending on the health or disease condition. Dysregulation of PCK may contribute to the development of obesity, cardiac hypertrophy, stroke, and cancer. Moreover, a regulatory network with multiple layers, from epigenetic regulation, transcription regulation, to posttranscription regulation, precisely tunes the expression of PCK. Deciphering the molecular basis that regulates PCK may pave the way for developing practical strategies to treat metabolic dysfunction.Major conclusionsIn this review, we summarize the metabolic and non-metabolic roles of the PCK enzyme in cells, especially beyond gluconeogenesis. We highlight the distinct functions of PCK isoforms (PCK1 and PCK2), depict a detailed network regulating PCK's expression, and discuss its clinical relevance. We also discuss the therapeutic potential targeting PCK and the future direction that is highly in need to better understand PCK-mediated signaling under diverse conditions.

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Gluconeogenesis in Leishmania mexicana: contribution of glycerol kinase, phosphoenolpyruvate carboxykinase, and pyruvate phosphate dikinase.

Project description:Gluconeogenesis is an active pathway in Leishmania amastigotes and is essential for their survival within the mammalian cells. However, our knowledge about this pathway in trypanosomatids is very limited. We investigated the role of glycerol kinase (GK), phosphoenolpyruvate carboxykinase (PEPCK), and pyruvate phosphate dikinase (PPDK) in gluconeogenesis by generating the respective Leishmania mexicana Δgk, Δpepck, and Δppdk null mutants. Our results demonstrated that indeed GK, PEPCK, and PPDK are key players in the gluconeogenesis pathway in Leishmania, although stage-specific differences in their contribution to this pathway were found. GK participates in the entry of glycerol in promastigotes and amastigotes; PEPCK participates in the entry of aspartate in promastigotes, and PPDK is involved in the entry of alanine in amastigotes. Furthermore, the majority of alanine enters into the pathway via decarboxylation of pyruvate in promastigotes, whereas pathway redundancy is suggested for the entry of aspartate in amastigotes. Interestingly, we also found that l-lactate, an abundant glucogenic precursor in mammals, was used by Leishmania amastigotes to synthesize mannogen, entering the pathway through PPDK. On the basis of these new results, we propose a revision in the current model of gluconeogenesis in Leishmania, emphasizing the differences between amastigotes and promastigotes. This work underlines the importance of studying the trypanosomatid intracellular life cycle stages to gain a better understanding of the pathologies caused in humans.

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Nur77 suppresses hepatocellular carcinoma via switching glucose metabolism toward gluconeogenesis through attenuating phosphoenolpyruvate carboxykinase sumoylation.

Project description:Gluconeogenesis, an essential metabolic process for hepatocytes, is downregulated in hepatocellular carcinoma (HCC). Here we show that the nuclear receptor Nur77 is a tumour suppressor for HCC that regulates gluconeogenesis. Low Nur77 expression in clinical HCC samples correlates with poor prognosis, and a Nur77 deficiency in mice promotes HCC development. Nur77 interacts with phosphoenolpyruvate carboxykinase (PEPCK1), the rate-limiting enzyme in gluconeogenesis, to increase gluconeogenesis and suppress glycolysis, resulting in ATP depletion and cell growth arrest. However, PEPCK1 becomes labile after sumoylation and is degraded via ubiquitination, which is augmented by the p300 acetylation of ubiquitin-conjugating enzyme 9 (Ubc9). Although Nur77 attenuates sumoylation and stabilizes PEPCK1 via impairing p300 activity and preventing the Ubc9-PEPCK1 interaction, Nur77 is silenced in HCC samples due to Snail-mediated DNA methylation of the Nur77 promoter. Our study reveals a unique mechanism to suppress HCC by switching from glycolysis to gluconeogenesis through Nur77 antagonism of PEPCK1 degradation.

| S-EPMC5333363 | biostudies-literature

Genetic Analysis of a Metazoan Pathway using Transcriptomic Phenotypes

Project description:RNA-seq is commonly used to identify genetic modules that respond to perturbations. In single cells, transcriptomes have been used as phenotypes, but this concept has not been applied to whole-organism RNA-seq. Linear models can quantify expression effects of individual mutants and identify epistatic effects in double mutants. However, interpreting these high-dimensional measurements is unintuitive. We developed a single coefficient to quantify transcriptome-wide epistasis which accurately reflects the underlying interactions. To demonstrate the power of our approach, we sequenced four single and two double Caenorhabditis elegans mutants. From these mutants, we successfully reconstructed the known hypoxia pathway. Using this approach, we uncovered a class of 31 genes that have opposing changes in expression in egl-9(lf) and vhl-1(lf) but for which the egl-9(lf);vhl-1(lf) mutant phenocopies egl-9(lf). These changes violate the classical model of HIF-1 regulation, but can be explained by postulating a role of hydroxylated HIF-1 in transcriptional control.

2017-04-04 | GSE97355 | GEO

Transcription profiling of HIF dependent and independent effects of VHL inactivation in C. elegans

Project description:The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function.

2013-01-30 | E-SMDB-23 | biostudies-arrayexpress

Gene expression under short-term moderate hypoxia and in the HIF-1 negative regulator mutants in Caenorhabditis elegans

Project description:Hypoxia inducible transcription factor HIF is the master regulator of hypoxia response in metazoans. The stability and activity of HIF are tightly regulated. In the model organism C. elegans, the homolog of HIF is HIF-1. The stability and activity of HIF-1 are negatively regulated by vhl-1, egl-9, rhy-1 and swan-1 when HIF-1 is stabilized by vhl-1 mutation. Here, we are using Affymetrix microarray to measure the immediate gene expression changes under short-term hypoxia treatment (2 hours of 0.5% oxygen treatment). We also want to understand whether the HIF-1 acvitity negative regulators function in common pathway(s) to regulate HIF-1 activity or not. We find that gene expression patterns in these HIF-1 activity negative regulator mutants are extraordinarily similar, which supports the model that they function in common pathway(s) to regulate HIF-1 activity.

2023-04-15 | GSE228851 | GEO

Loss of non-CpG methylation in inhibitory neurons impairs neural function through a mechanism that partially overlaps with Rett syndrome

Project description:Whole striatum were dissected from wild-type, as well as in mice where Dnmt3a or MeCP2 was conditional deleted in inhibitory neurons. Inhibitory neuronal nuclei were also conditionally tagged with GFP in all mice. Tissues were snap-frozen in liquid nitrogen until further analysis. Inhibitory neurons were sorted from whole striatum using anti-GFP-488 and anti-NeuN-647 signals and snap frozen until further analysis. Total DNA was purified from each sample using the DNeasy Blood & Tissue Kit from Qiagen according to manufactures instructions and stored at -20C until library preparation. DNA methylome libraries were generated using a modified snmC-seq method adapted for bulk DNA samples. Paired-end 150 cycle runs was used to sequence the libraries on a Illumina HiSeq 4000 Sequencing System.

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