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MOF haploinsufficiency triggers diet-induced obesity resistance

ABSTRACT: MOF haploinsufficiency triggers diet-induced obesity resistance

PROVIDER: PRJNA658027 | ENA |

REPOSITORIES: ENA

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MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

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MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

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MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

Project description:Constant crosstalk between epigenetic regulators and metabolism homeostasis ensures that several tissues can respond and adapt to environmental cues. Decreased levels of the lysine acetyltransferase (KAT), MOF, was recently associated with cerebral development and syndromic intellectual disability. However, the consequences of having a chronic reduction of MOF levels are still unveiled. Here we characterized by FIA-MS/MS the metabolic profile of Mof heterozygous animals. We generated the profile of 8 different organs that have distinct metabolic demands. Overall, our analysis revealed that Mof heterozygous mice have impaired glucose homeostasis, fatty acids metabolism, and amino acid accumulation. When exposed ad libitum to high-fat diet those animals failed to gain fat mass, while the lean mass remains unalterable. At the molecular level, using the adipocyte model we found that Mof regulates the expression of PPARs and Slc2a4. In summary, we identified the first KAT that shows high-fat diet resistance and we propose that the chronic reduction of Mof impacts metabolic disorders.

2021-07-23 | GSE154967 | GEO

MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

Project description:Constant crosstalk between epigenetic regulators and metabolism homeostasis ensures that several tissues can respond and adapt to environmental cues. Decreased levels of the lysine acetyltransferase (KAT), MOF, was recently associated with cerebral development and syndromic intellectual disability. However, the consequences of having a chronic reduction of MOF levels are still unveiled. Here we characterized by FIA-MS/MS the metabolic profile of Mof heterozygous animals. We generated the profile of 7 different organs that have distinct metabolic demands. Overall our analysis reveled that Mof heterozygous mice have impaired glucose homeostasis, fatty acids metabolism, and amino acid accumulation. Furthermore, when exposed ad libitum to high-fat diet those animals failed to gain fat mass, while the lean mass remains unalterable. Accordingly, at the molecular level, using the adipocyte model we found that Mof regulates the expression of PPARs and Slc2a4. In summary, we identified the first KAT that shows high-fat diet resistance and we propose that the chronic reduction of Mof has a strong impact on metabolic disorders.

2021-07-23 | GSE156462 | GEO

Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

Project description:Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

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MOF haploinsufficiency triggers diet-induced obesity resistance

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-23 | GSE156463 | GEO

Promoter or enhancer activation by CRISPRa rescues haploinsufficiency caused obesity

Project description:Haploinsufficiency, having only one functional copy of a gene, leads to a wide-range of human diseases. Using obesity as a disease model, we tested whether haploinsufficiency can be rescued by CRISPR-mediated activation (CRISPRa) of the normal allele. Haploinsufficiency of either SIM1 or MC4R, results in severe obesity in humans and mice. In transgenic mice, CRISPRa targeting of the Sim1 promoter or its ~270kb distant hypothalamic enhancer, rescued the obesity phenotype in Sim1 heterozygous mice. Interestingly, despite using a ubiquitous promoter for CRISPRa, Sim1 was upregulated only in tissues where the promoter or enhancer are active, suggesting that cis-regulatory elements can determine CRISPRa tissue-specificity. To evaluate the potential therapeutic use of CRISPRa, we injected CRISPRa-rAAV into the hypothalamus, leading to reversal of the obesity phenotype in Sim1 and Mc4r heterozygous mice. Our results show that CRISPRa can be developed as a gene regulation therapy (GRT) to treat altered gene dosage diseases.

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KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

Project description:KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

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Promoter or enhancer activation by CRISPRa rescues haploinsufficiency caused obesity

Project description:Promoter or enhancer activation by CRISPRa rescues haploinsufficiency caused obesity

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