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Genomic deletion of malic enzyme 2 confers collateral lethality in pancreas cancer

ABSTRACT: Comparison of malic enzyme 3 (ME3) depleted vs non-depleted xenograft tumors. ME3 is an isoform of ME2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80411 | GEO | 2017/08/22

SECONDARY ACCESSION(S): PRJNA318816

REPOSITORIES: GEO

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Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer.

Project description: Not available

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αKG-driven RNA polymerase II transcription of cyclin D1 licenses malic enzyme 2 to promote cell cycle progression

Project description:Increased metabolic activity usually provides energy and nutrients for biomass synthesis and is indispensable for the progression of the cell cycle. Here, we found an unexpected role for α-ketoglutarate (αKG) generation in regulating cell cycle gene transcription. A reduction in cellular αKG levels triggered by malic enzyme 2 (ME2) or isocitrate dehydrogenase 1 (IDH1) depletion leads to a pronounced arrest in G1 phase, while αKG supplementation promotes cell cycle progression. Mechanistically, αKG directly binds to RNA polymerase II (RNAPII), increasing the level of RNAPII binding to the cyclin D1 gene promoter, consequently enhancing cyclin D1 transcription. Notably, αKG addition is sufficient to restore cyclin D1 expression in ME2- or IDH1- depleted cells, facilitating cell cycle progression and proliferation in these cells. Therefore, our findings reveal a previously unappreciated function of αKG in gene transcriptional regulation and cell cycle control.

2023-06-25 | GSE221723 | GEO

Malic enzyme 2 mediates fumarate signaling to regulate mitochondrial biogenesis

Project description:Mitochondria have an independent genome (mtDNA) and protein synthesis machinery that coordinately activate for mitochondrial generation. Here, we report that Krebs cycle intermediate, fumarate, connects metabolism to mitobiogenesis through binding to malic enzyme 2 (ME2). Proteomic profiling of ME2-interacting protein reveals that ME2 binds to mitoribosome proteins to regulate mitoribosome assembly and mtDNA-encoded protein production. ME2 also interacts with and modulates deoxyuridine 5-triphosphate nucleotidohydrolase activity to regulate thymidine generation and mtDNA abundance

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The receptor-like cytosolic kinase RIPK activates NADP-malic enzyme 2 to generate NADPH for fueling the ROS production

Project description:Reactive oxygen species (ROS) production is a conserved immune response, primarily mediated in Arabidopsis by the respiratory burst oxidase homolog D (RBOHD), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase associated with the plasma membrane. A rapid increase in NADPH is necessary to fuel RBOHD proteins and hence maintain ROS production. However, the molecular mechanism underlying the NADPH generation for fueling RBOHD remains unclear. In this study, we isolated a new mutant allele of flagellin-insensitive 4 (FIN4), encoding the first enzyme in de novo NAD biosynthesis. fin4 mutants show reduced NADPH levels and impaired ROS production. However, FIN4 and other genes involved in the NAD- and NADPH-generating pathways are not highly upregulated upon elicitor treatment. Therefore, we hypothesized that a cytosolic NADP-linked dehydrogenase might be post-transcriptionally activated to keep the NADPH supply close to RBOHD. RPM1-INDUCED PROTEIN KINASE (RIPK), a receptor-like cytoplasmic kinase, regulates broad-spectrum ROS signaling in plant immunity. We then isolated the proteins associated with RIPK and identified NADP-malic enzyme 2 (NADP-ME2), an NADPH-generating enzyme. Compared with wild-type plants, nadp-me2 mutants display decreased NADP-ME activity, lower NADPH levels, as well as reduced ROS production in response to immune elicitors. Furthermore, we found that RIPK can directly phosphorylate NADP-ME2 and enhance its activity in vitro. The phosphorylation of NADP-ME2 S371 residue contributes to ROS production upon immune elicitor treatment and the susceptibility to the necrotrophic bacterium, Pectobacterium carotovorum. Overall, our study suggests that RIPK activates NADP-ME2 to rapidly increase cytosolic NADPH, hence fueling RBOHD to sustain ROS production in plant immunity.

2022-03-10 | GSE198017 | GEO

Liver gene expression profiling of cytosolic malic enzyme knockout mice

Project description:Cytosolic malic enzyme (Me1) was predicted as a causal gene for abdominal using a novel statistical method named LCMS (Schadt et al., 2005, Nature Genetics). In order to validate this prediction, we profiled the liver tissues of Me1 knockout mice (Me1-/-) and their littermate wild-type (wt) controls to examine the gene expression signature as well as pathways/networks resulting from the single gene perturbation.

2009-03-08 | GSE11992 | GEO

Liver gene expression profiling of cytosolic malic enzyme knockout mice

2009-03-07 | E-GEOD-11992 | biostudies-arrayexpress

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Histone lysine-to-methionine mutation reprograms the histone methylation landscape and contributes to pleiotropic development in Arabidopsis

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2017-06-16 | GSE92449 | GEO

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Project description:dKDM4A is a Drosophila H3 K9/K36 me2/me3 demethylase, which has been disrupted here by P-element insertion. We compare whole-genome ChIP-chip in mutant and WT to look for target genes of dKDM4A. Two samples, WT and dkDM4A mutant. 2 biological replicates each. 2 arrays.

2012-07-09 | E-GEOD-37016 | biostudies-arrayexpress

Comparing genome-wide H3K36me3 levels in WT vs. dKDM4A mutant

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