FOXQ1 Regulates Mitochondrial Cristae Formation and Energy Metabolism in Mouse Brain Endothelial Cells [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1133705 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29759188_1.fastq.gz | Fastqsanger.gz | |||
| SRR29759188_2.fastq.gz | Fastqsanger.gz | |||
| SRR29759189_1.fastq.gz | Fastqsanger.gz | |||
| SRR29759189_2.fastq.gz | Fastqsanger.gz | |||
| SRR29759190_1.fastq.gz | Fastqsanger.gz |
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Project description:FOXQ1 Regulates Mitochondrial Cristae Formation and Energy Metabolism in Mouse Brain Endothelial Cells [CUT&TAG]
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Project description:To explore FOXQ1’s transcriptional role, we utilized an HA-tagged FOXQ1 plasmid for CUTTag enabling high-resolution mapping of FOXQ1 binding sites on the genome.
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Project description:Purpose: To gain futher insight into how FOXQ1 regulates the brain endothelial cells ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortical endothelial cells of E18 FOXQ1 conditional knock out mice and littermate wild-type. Methods: Total RNA from E18 Flow sorting of endothelial cells of wild-type(WT) and FOXQ1fl/fl;Tie2-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 6000 platform in Annoroad Genomics Approximately one thousand transcripts showed differential expression between the wild-type(WT) and FOXQ1fl/fl;Tie2-Cre mice cortical endothelial cells, with a fold change ≥1.5 and p value <0.05. These results reflected FOXQ1 plays a role in brain endothelial cells. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how FOXQ1 works in endothelial cells.
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Project description:Mitochondrial damage causes mtDNA release to activate type I interferon (IFN-I) response via the cGAS-STING pathway. mtDNA-induced inflammation promotes autoimmune and aging-related degenerative disorders. However, the global picture of inflammation-inducing mitochondrial damages remains obscure. Here we performed a mitochondria-targeted CRISPR-knockout screen for regulators of the IFN-I response. Strikingly, our screen revealed dozens of hits enriched with key regulators of cristae architecture, including phospholipid cardiolipin and protein complexes such as OPA1, MICOS, SAM, MIB, PHB, and the F1Fo-ATP synthase. Disrupting these cristae organizers consistently induced mtDNA release and STING-dependent IFN-I response. Furthermore, robust STING-dependent IFN-I response was induced in vivo by knocking out MTX2, a subunit of the SAM complex whose null-mutations cause progeria in human. Taken together, beyond revealing the central role of cristae architecture to prevent mtDNA release and inflammation, our results mechanistically link mitochondrial cristae disorganization and inflammation, two emerging hallmarks of aging and aging-related degenerative diseases.
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Project description:The mitochondrial contact site and cristae organization system (MICOS) is a complex responsible for proper cristae formation. Empirical data about this ubiquitous complex is limited to opisthokont models (e.g. yeast), impeding understanding of its core properties and adaptation potential to diverse cellular milieus. To close this knowledge gap, we characterized MICOS from the diverged excavate Trypanosoma brucei. These results allow the definition of fundamental MICOS properties, such as its role in maintaining both cristae and contacts between the inner and outer membranes plus its extrusion into the intermembrane space. Yet, surprising differences with opisthokonts indicate that MICOS can assume different forms. T. brucei MICOS contains a novel subunit involved in the import of intermembrane space proteins, including respiratory chain complex assembly factors. We propose an evidence-based hypothesis that T. brucei MICOS populates cristae membranes with proteins needed for respiration, supported by the complex's even distribution in cristae
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Project description:Mitochondrial cristae architecture protects against mtDNA release and inflammation
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Project description:The detachment of epithelial cells, but not cancer cells, causes anoikis due to reduced energy production. Invasive tumor cells generate three splice variants of the metastasis gene osteopontin. The cancer-specific form osteopontin-c supports anchorage-independence through inducing oxidoreductases and upregulating intermediates/enzymes in the hexose monophosphate shunt, glutathione cycle, glycolysis, glycerol phosphate shuttle, and mitochondrial respiratory chain. Osteopontin-c signaling upregulates glutathione (consistent with the induction of the enzyme GPX-4), glutamine and glutamate (which can feed into the tricarboxylic acid cycle). Consecutively, the cellular ATP levels are elevated. The elevated creatine may be synthesized from serine via glycine and also supports the energy metabolism by increasing the formation of ATP. Metabolic probing with N-acetyl-L-cysteine, L-glutamate, or glycerol identified differentially regulated pathway components, with mitochondrial activity being redox dependent and the creatine pathway depending on glutamine. The effects are consistent with a stimulation of the energy metabolism that supports anti-anoikis. Our findings imply a synergism in cancer cells between osteopontin-a, which increases the cellular glucose levels, and osteopontin-c, which utilizes this glucose to generate energy. mRNA profiles of MCF-7 cells transfected with osteopontin-a, osteopontin-c and vector control were generated by RNA-Seq, in triplicate, by Illumina HiSeq.
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Project description:OTUD3 regulates energy metabolism
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Project description:Mitochondrial cristae are polymorphic invaginations of the inner membrane that are the fabric of cellular respiration. Both the Mitochondrial Contact Site and Cristae Organization System (MICOS) and the F1FO-ATP synthase are vital for sculpting cristae by opposing membrane bending forces. While MICOS promotes negative curvature at cristae junctions, dimeric F1FO-ATP synthase is crucial for positive curvature at cristae rims. Crosstalk between these two complexes has been observed in baker’s yeast, the model organism of the Opisthokonta supergroup. Here, we report that this property is conserved in Trypanosoma brucei, a member of the Discoba supergroup that separated from Opisthokonta ~2 billion years ago. Specifically, one of the paralogs of the core MICOS subunit Mic10 interacts with dimeric F1FO-ATP synthase, whereas the other core Mic60 subunit has a counteractive effect on F1FO-ATP synthase oligomerization. This is evocative of the nature of MICOS-F1FO-ATP synthase crosstalk in yeast, which is remarkable given the diversification these two complexes have undergone during almost 2 eons of independent evolution. Furthermore, we identified a highly diverged trypanosome homolog of subunit e, which is essential for the stability of F1FO-ATP synthase dimers in yeast. Just like subunit e, it is preferentially associated with dimers, interacts with Mic10 and its silencing results in severe defects to cristae and disintegration of F1FO-ATP synthase dimers. Our findings indicate that crosstalk between MICOS and dimeric F1FO-ATP synthase is a fundamental property impacting cristae shape throughout eukaryotes.
2021-06-15 | PXD025109 | Pride
Project description:The detachment of epithelial cells, but not cancer cells, causes anoikis due to reduced energy production. Invasive tumor cells generate three splice variants of the metastasis gene osteopontin. The cancer-specific form osteopontin-c supports anchorage-independence through inducing oxidoreductases and upregulating intermediates/enzymes in the hexose monophosphate shunt, glutathione cycle, glycolysis, glycerol phosphate shuttle, and mitochondrial respiratory chain. Osteopontin-c signaling upregulates glutathione (consistent with the induction of the enzyme GPX-4), glutamine and glutamate (which can feed into the tricarboxylic acid cycle). Consecutively, the cellular ATP levels are elevated. The elevated creatine may be synthesized from serine via glycine and also supports the energy metabolism by increasing the formation of ATP. Metabolic probing with N-acetyl-L-cysteine, L-glutamate, or glycerol identified differentially regulated pathway components, with mitochondrial activity being redox dependent and the creatine pathway depending on glutamine. The effects are consistent with a stimulation of the energy metabolism that supports anti-anoikis. Our findings imply a synergism in cancer cells between osteopontin-a, which increases the cellular glucose levels, and osteopontin-c, which utilizes this glucose to generate energy.
2014-02-21 | GSE55193 | GEO