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Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Schmidtea mediterranea

PROVIDER: GSE134302 | GEO | 2020/11/15

REPOSITORIES: GEO

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Tnfaip2/exoc3-driven lipid metabolism is essential for stem cell differentiation and organ homeostasis.

Project description:Lipid metabolism influences stem cell maintenance and differentiation but genetic factors that control these processes remain to be delineated. Here, we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout impairs differentiation of embryonic stem cells (ESCs), and knockdown of the planarian para-ortholog, Smed-exoc3, abrogates in vivo tissue homeostasis and regeneration-processes that are driven by somatic stem cells. When stimulated to differentiate, Tnfaip2-deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of vimentin (Vim)-a known inducer of LD formation. Smed-exoc3 depletion also causes a strong reduction of TAGs in planarians. The study shows that Tnfaip2 acts epistatically with and upstream of Vim in impairing cellular reprogramming. Supplementing palmitic acid (PA) and palmitoyl-L-carnitine (the mobilized form of PA) restores the differentiation capacity of Tnfaip2-deficient ESCs and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel role of Tnfaip2 and exoc3 in controlling lipid metabolism, which is essential for ESC differentiation and planarian organ maintenance.

| S-EPMC7788457 | biostudies-literature

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Schmidtea mediterranea]

Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.

2020-11-16 | GSE134300 | GEO

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Mus musculus, 1]

2020-11-16 | GSE134301 | GEO

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Mus musculus, 2]

2020-11-16 | GSE148758 | GEO

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis

Project description:Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis

| PRJNA554666 | ENA

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Schmidtea mediterranea]

Project description:Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Schmidtea mediterranea]

| PRJNA554667 | ENA

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Mus musculus, 1]

Project description:Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Mus musculus, 1]

| PRJNA554668 | ENA

Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Mus musculus, 2]

Project description:Tnfaip2/Exoc3 driven lipid metabolism is essential for stem cell differentiation & organ homeostasis [Mus musculus, 2]

| PRJNA625650 | ENA

ABHD11 Is Critical for Embryonic Stem Cell Expansion, Differentiation and Lipid Metabolic Homeostasis.

Project description:Growing evidence supports the notion that lipid metabolism is critical for embryonic stem cell (ESC) maintenance. Recently, α/β-hydrolase domain-containing (ABHD) proteins have emerged as novel pivotal regulators in lipid synthesis or degradation while their functions in ESCs have not been investigated. In this study, we revealed the role of ABHD11 in ESC function using classical loss and gain of function experiments. Knockout of Abhd11 hampered ESC expansion and differentiation, triggering the autophagic flux and apoptosis. In contrast, Abhd11 overexpression exerted anti-apoptotic effects in ESCs. Moreover, Abhd11 knockout disturbed GSK3β/β-Catenin and ERK signaling transduction. Finally, Abhd11 knockout led to the misexpression of key metabolic enzymes related to lipid synthesis, glycolysis, and amino acid metabolism, and ABHD11 contributed to the homeostasis of lipid metabolism. These findings provide new insights into the broad role of ABHD proteins and highlight the significance of regulators of lipid metabolism in the control of stem cell function.

| S-EPMC7358615 | biostudies-literature

Regulatory T cell differentiation is controlled by αKG-induced alterations in mitochondrial metabolism and lipid homeostasis.

Project description:Suppressive regulatory T cell (Treg) differentiation is controlled by diverse immunometabolic signaling pathways and intracellular metabolites. Here we show that cell-permeable α-ketoglutarate (αKG) alters the DNA methylation profile of naive CD4 T cells activated under Treg polarizing conditions, markedly attenuating FoxP3+ Treg differentiation and increasing inflammatory cytokines. Adoptive transfer of these T cells into tumor-bearing mice results in enhanced tumor infiltration, decreased FoxP3 expression, and delayed tumor growth. Mechanistically, αKG leads to an energetic state that is reprogrammed toward a mitochondrial metabolism, with increased oxidative phosphorylation and expression of mitochondrial complex enzymes. Furthermore, carbons from ectopic αKG are directly utilized in the generation of fatty acids, associated with lipidome remodeling and increased triacylglyceride stores. Notably, inhibition of either mitochondrial complex II or DGAT2-mediated triacylglyceride synthesis restores Treg differentiation and decreases the αKG-induced inflammatory phenotype. Thus, we identify a crosstalk between αKG, mitochondrial metabolism and triacylglyceride synthesis that controls Treg fate.

| S-EPMC10167917 | biostudies-literature

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