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The lipid handling capacity of subcutaneous fat is programmed by mTORC2 during development

ABSTRACT: The lipid handling capacity of subcutaneous fat is programmed by mTORC2 during development

PROVIDER: PRJNA610622 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11245734_1.fastq.gz	Fastqsanger.gz
	SRR11245734_2.fastq.gz	Fastqsanger.gz
	SRR11245735_1.fastq.gz	Fastqsanger.gz
	SRR11245735_2.fastq.gz	Fastqsanger.gz
	SRR11245736_1.fastq.gz	Fastqsanger.gz

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The lipid handling capacity of subcutaneous fat is programmed by mTORC2 during development

Project description:Obesity causes type 2 diabetes, cardiovascular diseases, NAFLD, and cancer, but all fat is not equal as subcutaneous white adipose tissue (SWAT) is more metabolically favorable than visceral fat. Here, we investigate mTORC2 function in SWAT growth by deleting its essential subunit Rictor in SWAT precursor cells and examining its effect on adipocyte differentiation and tissue development. We found that Rictor/mTORC2 is not required for SWAT preadipocyte differentiation per se; however, SWAT preadipocytes differentiating without Rictor cannot fully induce the lipid storage transcriptional program. In vivo, this results in smaller adipocytes, reduced SWAT size, lipid re-distribution to visceral and brown fat, and gender-distinct effects on systemic metabolic fitness. Mechanistically, mTORC2 promotes PPARg activity towards specific lipid metabolism genes independently of ChREBP, but in coordination, to set the lipid handling capacity of SWAT. Further exploring this pathway may uncover new strategies to stimulate lipid storage in more metabolically favorable SWAT.

2020-10-06 | GSE146470 | GEO

The Lipid Handling Capacity of Subcutaneous Fat Is Programmed by mTORC2 during Development.

Project description:Overweight and obesity are associated with type 2 diabetes, non-alcoholic fatty liver disease, cardiovascular disease and cancer, but all fat is not equal, as storing excess lipid in subcutaneous white adipose tissue (SWAT) is more metabolically favorable than in visceral fat. Here, we uncover a critical role for mTORC2 in setting SWAT lipid handling capacity. We find that subcutaneous white preadipocytes differentiating without the essential mTORC2 subunit Rictor upregulate mature adipocyte markers but develop a striking lipid storage defect resulting in smaller adipocytes, reduced tissue size, lipid re-distribution to visceral and brown fat, and sex-distinct effects on systemic metabolic fitness. Mechanistically, mTORC2 promotes transcriptional upregulation of select lipid metabolism genes controlled by PPARγ and ChREBP, including genes that control lipid uptake, synthesis, and degradation pathways as well as Akt2, which encodes a major mTORC2 substrate and insulin effector. Further exploring this pathway may uncover new strategies to improve insulin sensitivity.

| S-EPMC7607535 | biostudies-literature

Epigenome analysis of control and mTORC2-suppressed glioblastoma cells

Project description:Genome wide DNA methylation profiling of control and mTORC2-suppressed glioblastoma cells (U87-EGFRvIII cells). The Illumina Infinium HumanMethylation EPIC BeadChip Array was used to obtain DNA methylation profiles with 865,918 probes in glioblastoma cell line samples. Samples included 2 control U87-MG cells without mTORC2 suppresion, and mTORC2-knockdown U87-MG cells with lentivirus-mediated suppression of mTORC2.

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screen miRNAs specifically regulated by mTORC1 or mTORC2

Project description:To screen miRNAs specifically regulated by mTORC1 or mTORC2, a global miRNA expression profile in MCF-7 cells treated with rapamycin or PP242 (mTORC1/2 kinase inhibitor) was developed using microarray. control, rapamycin or PP242 treated human MCF-7 cells were harvested 48h post-treatment and subjected to total RNA extraction.

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mTORC2-mediated cell-cell interaction promote BMP4-induced WNT activation and mesoderm differentiation

Project description:The mechanistic target of rapamycin complex 2 (mTORC2) is essential for embryonic development but the underlying molecular mechanisms remain unclear. Here we show that disruption of mTORC2 in human embryonic stem cells (hESCs) considerably alters the balance of Rho/Rac signaling and reduces cell adhesion. Although these changes have no clear effect on their self-renewal and the expression of pluripotent markers, they significantly impede BMP-induced activation of canonical WNT genes, leading to impaired mesendoderm differentiation. Direct activation of the downstream WNT pathway by inhibiting GSK3 dramatically improves mesendoderm differentiation in mTORC2-deficient hESCs. Our studies uncover a new mechanism by which mTORC2 regulates cell fate determination and link the intercellular contacts with the activation of WNT genes.

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Project description:The mTOR pathway orchestrates cellular homeostasis. The rapamycin-sensitive mTOR complex (mTORC1) in the kidney has been widely studied; however, mTORC2 function in renal tubules is poorly characterized. Here, we generated mice lacking mTORC2 in the distal tubule (Rictorfl/fl Ksp-Cre mice), which were viable and had no obvious phenotype, except for a 2.5-fold increase in plasma aldosterone. Challenged with a low-Na+ diet, these mice adequately reduced Na+ excretion; however, Rictorfl/fl Ksp-Cre mice rapidly developed hyperkalemia on a high-K+ diet, despite a 10-fold increase in serum aldosterone levels, implying that mTORC2 regulates kaliuresis. Phosphorylation of serum- and glucocorticoid-inducible kinase 1 (SGK1) and PKC-α was absent in Rictorfl/fl Ksp-Cre mice, indicating a functional block in K+ secretion activation via ROMK channels. Indeed, patch-clamp experiments on split-open tubular segments from the transition zone of the late connecting tubule and early cortical collecting duct demonstrated that Ba2+-sensitive apical K+ currents were barely detectable in the majority of Rictorfl/fl Ksp-Cre mice. Conversely, epithelial sodium channel (ENaC) activity was largely preserved, suggesting that the reduced ability to maintain K+ homeostasis is the result of impaired apical K+ conductance and not a reduced electrical driving force for K+ secretion. Thus, these data unravel a vital and nonredundant role of mTORC2 for distal tubular K+ handling.

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Genome-wide maps of chromatin H3K9ac state in control and mTORC2-suppressed glioblastoma cells

Project description:We herein demonstrate that mammalian target of rapamycin complex 2 (mTORC2), a critical core component of the growth factor signaling system, globally alters histone acetylation through metabolic reprogramming in the highly malignant brain tumor glioblastoma (GBM). Integrated analyses unravel that mTORC2 regulates iron trafficking via histone H3K9 acetylation of the ferritin promoter, facilitating GBM growth and survival. These findings nominate mTORC2 as a critical epigenetic regulator of iron metabolism in cancer.

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