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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

ABSTRACT: 2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

PROVIDER: PRJNA1259937 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33458675_1.fastq.gz	Fastqsanger.gz
	SRR33458675_2.fastq.gz	Fastqsanger.gz
	SRR33458676_1.fastq.gz	Fastqsanger.gz
	SRR33458676_2.fastq.gz	Fastqsanger.gz
	SRR33458677_1.fastq.gz	Fastqsanger.gz

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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

Project description:2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

Project description:This study reports accumulation of larger lipid droplets in an adipocyte specific manner upon loss of CLPP. The mitochondria in KO BAT have mild respiratory chain deficiency but no difference in respiratory output at tissue and cellular level. Omics analysis reveals that loss of CLPP leads to tissue remodeling, and is accompanied by pertinent cytoskeletal changes. The metabolite, 2-hydroxyglutarate accumulates in KO tissue and cells and is possibly produced by the moonlighting function of PHGDH. We further identify 2-HG H3K4me3 methylation changes in epigenome being likely contributing to larger lipid droplets. The study also reports that 2HG mediated whitning is coupled to nuclear softening and changes in nuclear mechanics.

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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction II

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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction II

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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

Project description:Mitochondria play a crucial role in regulating cellular homeostasis in response to intrinsic and extrinsic cues by changing cellular metabolism to meet these challenges. However, the molecular underpinnings of this regulation and the complete spectrum of these physiological outcomes remain largely unexplored. In this study, we elucidate the mechanisms driving the whitening phenotype in brown adipose tissue (BAT) deficient in the mitochondrial matrix protease CLPP. We find that CLPP-deficient BAT shows aberrant accumulation of lipid droplets, which occurs independently of defects in oxygen consumption and fatty acid oxidation. Our results indicate that mitochondrial dysfunction due to CLPP deficiency leads to the build-up of the oncometabolite 2-hydroxyglutarate (2-HG), which in turn promotes lipid droplet enlargement. We further demonstrate that 2-HG influences gene expression and decreases nuclear stiffness by modifying epigenetic signatures. We propose that lipid accumulation and altered nuclear stiffness regulated through 2-HG are novel stress responses to mitochondrial dysfunction.

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2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction

Project description:Mitochondria play a crucial role in regulating cellular homeostasis in response to intrinsic and extrinsic cues by changing cellular metabolism to meet these challenges. However, the molecular underpinnings of this regulation and the complete spectrum of these physiological outcomes remain largely unexplored. In this study, we elucidate the mechanisms driving the whitening phenotype in brown adipose tissue (BAT) deficient in the mitochondrial matrix protease CLPP. We find that CLPP-deficient BAT shows aberrant accumulation of lipid droplets, which occurs independently of defects in oxygen consumption and fatty acid oxidation. Our results indicate that mitochondrial dysfunction due to CLPP deficiency leads to the build-up of the oncometabolite D-2hydroxyglutarate (D-2HG), which in turn promotes lipid droplet enlargement. We further demonstrate that D-2HG influences gene expression and decreases nuclear stiffness by modifying epigenetic signatures. We propose that lipid accumulation and altered nuclear stiffness regulated through 2-HG are unique stress responses to mitochondrial dysfunction.

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Project description:Brown adipose tissue (BAT) is a highly vascularized organ with abundant mitochondria that produce heat through uncoupled respiration. Obesity is associated with a reduction of BAT function; however, it is unknown how obesity promotes dysfunctional BAT. Here, using a murine model of diet-induced obesity, we determined that obesity causes capillary rarefaction and functional hypoxia in BAT, leading to a BAT “whitening” phenotype that is characterized by mitochondrial dysfunction, lipid droplet accumulation, and decreased expression of Vegfa. Targeted deletion of Vegfa in adipose tissue of nonobese mice resulted in BAT whitening, supporting a role for decreased vascularity in obesity-associated BAT. Conversely, introduction of VEGF-A specifically into BAT of obese mice restored vascularity, ameliorated brown adipocyte dysfunction, and improved insulin sensitivity. The capillary rarefaction in BAT that was brought about by obesity or Vegfa ablation diminished β-adrenergic signaling, increased mitochondrial ROS production, and promoted mitophagy. These data indicate that overnutrition leads to the development of a hypoxic state in BAT, causing it to whiten through mitochondrial dysfunction and loss. Furthermore, these results link obesity-associated BAT whitening to impaired systemic glucose metabolism.

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DJ1 ablation enhances CMA activity to exacerbate BAT whitening in humanized mice

Project description:Humans predominantly live under thermoneutral conditions, leading to brown adipose tissue (BAT) whitening, a reduction in mitochondrial content and thermogenesis. Here, the adaptations to thermal stress of BAT are examined using quantitative proteomics, finding that Parkinson’s disease (PD) pathways are sensitive to ambient temperature. Ablation of DJ-1, a PD gene, exaggerates BAT whitening, resulting in impaired insulin sensitivity and energy expenditure at thermoneutrality. We further identify that the activity of chaperon-mediated autophagy (CMA) contributes to the deletion of DJ-1-induced metabolic phenotypes. Importantly, DJ-1 interacts with HSC70 and subsequently decreases the activity of CMA, enhances the stability of thermogenic proteins. Moreover, inhibiting the activity of CMA by knockdown of LAMP2A counteracts the phenotypes induced by DJ-1 ablation. Additionally, while 4-PBA, an agonist of DJ-1, upregulates mitochondrial oxygen consumption; compound 23, an antagonist of DJ-1, exerts the opposite effects. Collectively, these data address a cell-autonomous route to regulate BAT whitening at thermoneutrality.

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