Remodeling of white fat during browning involves YBX1 to drive thermogenic commitment
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ABSTRACT:
PROVIDER: PRJNA627345 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11586908_1.fastq.gz | Fastqsanger.gz | |||
| SRR11586908_2.fastq.gz | Fastqsanger.gz | |||
| SRR11586909_1.fastq.gz | Fastqsanger.gz | |||
| SRR11586909_2.fastq.gz | Fastqsanger.gz | |||
| SRR11586910_1.fastq.gz | Fastqsanger.gz |
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Project description:Effects of YBX1 activation in PPARγ-indcuded C3H/10T1/2-SAM pre-adipocytes on the transcriptome of cells during early differentation stages
2021-01-11 | GSE149083 | GEO
Project description:ObjectiveIncreasing adaptive thermogenesis by stimulating browning in white adipose tissue is a promising method of improving metabolic health. However, the molecular mechanisms underlying this transition remain elusive. Our study examined the molecular determinants driving the differentiation of precursor cells into thermogenic adipocytes.MethodsIn this study, we conducted temporal high-resolution proteomic analysis of subcutaneous white adipose tissue (scWAT) after cold exposure in mice. This was followed by loss- and gain-of-function experiments using siRNA-mediated knockdown and CRISPRa-mediated induction of gene expression, respectively, to evaluate the function of the transcriptional regulator Y box-binding protein 1 (YBX1) during adipogenesis of brown pre-adipocytes and mesenchymal stem cells. Transcriptomic analysis of mesenchymal stem cells following induction of endogenous Ybx1 expression was conducted to elucidate transcriptomic events controlled by YBX1 during adipogenesis.ResultsOur proteomics analysis uncovered 509 proteins differentially regulated by cold in a time-dependent manner. Overall, 44 transcriptional regulators were acutely upregulated following cold exposure, among which included the cold-shock domain containing protein YBX1, peaking after 24 h. Cold-induced upregulation of YBX1 also occurred in brown adipose tissue, but not in visceral white adipose tissue, suggesting a role of YBX1 in thermogenesis. This role was confirmed by Ybx1 knockdown in brown and brite preadipocytes, which significantly impaired their thermogenic potential. Conversely, inducing Ybx1 expression in mesenchymal stem cells during adipogenesis promoted browning concurrent with an increased expression of thermogenic markers and enhanced mitochondrial respiration. At a molecular level, our transcriptomic analysis showed that YBX1 regulates a subset of genes, including the histone H3K9 demethylase Jmjd1c, to promote thermogenic adipocyte differentiation.ConclusionOur study mapped the dynamic proteomic changes of murine scWAT during browning and identified YBX1 as a novel factor coordinating the genomic mechanisms by which preadipocytes commit to brite/beige lineage.
| S-EPMC7779825 | biostudies-literature
Project description:In order to identify YBX1 binding sites on endogenous RNA, we performed HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Licatalosi D, et al. 2008, Nature 456:464-U22)
2015-05-08 | E-GEOD-63604 | biostudies-arrayexpress
Project description:The adipose tissue is a key site regulating energy metabolism. One of the contributing factors behind this is browning of white adipose tissue (WAT), however, knowledge of the intracellular determinants of browning process remains incomplete. By generating adipocyte-specific Senp2 knockout (Senp2-aKO) mice, here we showed that SENP2 negatively regulates browning by de-conjugating SUMO from C/EBPβ. Senp2-aKO mice were resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and heat production. Senp2 knockout promoted beige adipocyte accumulation in inguinal WAT by upregulation of thermogenic gene expression. In addition, SENP2 knockdown promoted thermogenic adipocyte differentiation of precursor cells isolated from inguinal and epididymal WATs. Mechanistically, sumoylated C/EBPβ, a target of SENP2, suppressed expression of HOXC10, a browning inhibitor, by recruiting a transcriptional repressor DAXX. These findings indicate that a SENP2-C/EBPβ-HOXC10 axis operates for the control of beige adipogenesis in inguinal WAT.
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Project description:The adipose tissue is a key site regulating energy metabolism. One of the contributing factors behind this is browning of white adipose tissue (WAT), however, knowledge of the intracellular determinants of browning process remains incomplete. By generating adipocyte-specific Senp2 knockout (Senp2-aKO) mice, here we showed that SENP2 negatively regulates browning by de-conjugating SUMO from C/EBPβ. Senp2-aKO mice were resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and heat production. Senp2 knockout promoted beige adipocyte accumulation in inguinal WAT by upregulation of thermogenic gene expression. In addition, SENP2 knockdown promoted thermogenic adipocyte differentiation of precursor cells isolated from inguinal and epididymal WATs. Mechanistically, sumoylated C/EBPβ, a target of SENP2, suppressed expression of HOXC10, a browning inhibitor, by recruiting a transcriptional repressor DAXX. These findings indicate that a SENP2-C/EBPβ-HOXC10 axis operates for the control of beige adipogenesis in inguinal WAT.
2023-11-27 | GSE189387 | GEO
Project description:In order to identify YBX1 binding sites on tRNA fragments, we performed small-RNA HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Chi SW, et al. 2009, Nature 460:479)
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Project description:YBX1 is a multifunctional protein involved in the control of transcription and translation. We identified YBX1 as an target of MEK/ERK signaling in colorectal cancer cell lines. We performed a ChIP-chip analysis of HCT116 cells to identify new potential target genes of YBX1. Comparison of input DNA fragments with fragments coprecipitated with YBX1 in HCT116 cells.
2010-10-09 | E-GEOD-18337 | biostudies-arrayexpress
Project description:In order to identify YBX1-dependent targets that are modulated under hypoxic conditions, we used control and YBX1 knockdown cells grown under normoxia and hypoxia to profile gene expression levels. Control and YBX1-knockdown cells were grown and profiled under hypoxia and normoxia to identify YBX1-dependent hypoxia-induced target transcripts.
2015-05-08 | E-GEOD-63562 | biostudies-arrayexpress
Project description:In order to identify YBX1-dependent targets that are modulated upon changing the levels of endogenous tRFs, we used transient transfection of antisense locked-nucleic acids (LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr followed by microarray profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected into control and YBX1-knockdown cells to identify YBX1-dependent targets that are modulated due to tRF loss-of-function.
2015-05-08 | E-GEOD-63564 | biostudies-arrayexpress
Project description:Mechanisms that control “beige/brite” thermogenic adipose tissue development may be harnessed to improve human metabolic health. To define these mechanisms, we developed a species-hybrid model in which human mesenchymal progenitor cells were used to develop white or thermogenic/beige adipose tissue in mice. The hybrid adipose tissue developed distinctive features of human adipose tissue, such as larger adipocyte size, despite its neurovascular architecture being entirely of murine origin. Thermogenic adipose tissue recruited a denser, qualitatively distinct vascular network, differing in genes mapping to circadian rhythm pathways, and denser sympathetic innervation. The enhanced thermogenic neurovascular network was associated with human adipocyte expression of THBS4, TNC, NTRK3 and SPARCL1, which enhance neurogenesis, and decreased expression of MAOA and ACHE, which control neurotransmitter tone. Systemic inhibition of MAOA, which is present in human but absent in mouse adipocytes, induced browning of human but not mouse adipose tissue, revealing the physiological relevance of this pathway. Our results reveal species-specific cell type dependencies controlling the development of thermogenic adipose tissue and point to human adipocyte MAOA as a potential target for metabolic disease therapy.
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