Expression profile in WAT from inducible adipocyte specific TFG KO mice
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ABSTRACT:
PROVIDER: PRJNA602366 | ENA |
REPOSITORIES: ENA
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Project description:The expression of Trk-fused gene (TFG) was markedly increased in adipose tissues from ob/ob mice. To examine the function of TFG in adipocytes, we performed microarray analysis using the Affymetrics Clariom D Array, Mouse.
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Project description:Circulating trimethylamine N-oxide (TMAO) participates in the pathogenesis of cardio-metabolic diseases, with hepatic flavin-containing monooxygenase 3 (FMO3) originally regarded as the primary source of TMAO production. Here, we demonstrate that white adipose tissue (WAT) expressed FMO3 and its derived metabolic product TMAO causatively contribute to the systemic elevation of TMAO levels, WAT dysfunction, and metabolic diseases in ageing. We showed that FMO3 expression and TMAO levels are upregulated in WAT of naturally ageing animals and human subjects, as well as in a DNA damage-induced senescent adipocyte model, but not in the liver. This upregulation is due to p53 activation in mice and could be mitigated by calorie restriction in humans. Adipocyte-specific ablation of FMO3 attenuates TMAO accumulation in WAT and circulation, leading to enhanced glucose metabolism, energy homeostasis, and lipid regulation in aged and high-fat diet-induced obese mice. Transcriptomic and histological analysis link these metabolic improvements to reduced senescence, fibrosis, and inflammation in WAT as well as a decrease in adipose-resident macrophages. LiP-small molecule mapping (LiP-SMap) analysis identified numerous novel TMAO-interacting proteins implicated in inflammasome activation within white adipocytes and macrophages. Mechanistically, TMAO facilitates inflammasome activation by binding to the inflammasome adaptor protein apoptosis-associated speck-like protein containing A CARD (ASC), thereby inducing its expression, caspase-1 activation, and subsequent interleukin-1β (IL-1β) production. Our findings uncover a pivotal role for adipocyte FMO3 in modulating TMAO production and WAT dysfunction by promoting inflammasome activation in ageing via an autocrine and paracrine manner.
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Project description:The diverse transcriptional mechanisms governing cellular differentiation and development of mammalian tissue remains poorly understood. Here we report that TAF7L, a paralogue of TFIID subunit TAF7, is enriched in adipocytes and mouse white fat tissue (WAT). Depletion of TAF7L reduced adipocyte-specific gene expression and compromised adipocyte differentiation as well as WAT development. Ectopic expression of TAF7L in myoblasts reprograms these muscle precursors into adipocytes upon induction. Genome-wide mRNA-seq expression profiling and ChIP-seq binding studies confirmed that TAF7L is required for activating adipocyte-specific genes via a dual mechanism wherein it interacts with PPARM-NM-3 at enhancers and TBP/Pol II at core promoters. In vitro binding studies confirmed that TAF7L forms complexes with both TBP and PPARM-NM-3. These findings suggest that TAF7L plays an integral role in adipocyte gene expression by targeting enhancers as a cofactor for PPARM-NM-3 and promoters as a component of the core transcriptional machinery. Genome-wide mapping of TAF7L and additional factors, and mRNA-seq expression profiling prior to and following mouse adipocyte differentiation.
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