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Osteoprotection through the deletion of the transcription factor Rorβ in mice

ABSTRACT: Osteoprotection through the deletion of the transcription factor Rorβ in mice

PROVIDER: PRJNA421705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6363043_1.fastq.gz	Fastqsanger.gz
	SRR6363043_2.fastq.gz	Fastqsanger.gz
	SRR6363044_1.fastq.gz	Fastqsanger.gz
	SRR6363044_2.fastq.gz	Fastqsanger.gz
	SRR6363045_1.fastq.gz	Fastqsanger.gz

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Osteoprotection Through the Deletion of the Transcription Factor Ror? in Mice.

Project description:There is a clinical need to identify new molecular targets for the treatment of osteoporosis, particularly those that simultaneously inhibit bone resorption while stimulating bone formation. We have previously shown in overexpression studies that retinoic acid receptor-related orphan receptor ? (Ror?) suppresses in vitro osteoblast differentiation. In addition, the expression of Ror? is markedly increased in bone marrow-derived mesenchymal stromal cells with aging in both mice and humans. Here we establish a critical role for Ror? in regulating bone metabolism using a combination of in vitro and in vivo studies. We used Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 gene editing to demonstrate that loss of Ror? in osteoblasts enhances Wnt signaling, specifically through increased recruitment of ?-catenin to T-cell factor/lymphoid enhancer factor (Tcf/Lef) DNA binding sites in the promoters of the Wnt target genes Tcf7 and Opg. This resulted in increased osteogenic gene expression and suppressed osteoclast formation through increased osteoprotegerin (OPG) secretion in Ror?-deficient cells. Consistent with our in vitro data, genetic deletion of Ror? in both female and male mice resulted in preserved bone mass and microarchitecture with advancing age due to increased bone formation with a concomitant decrease in resorption. The improved skeletal phenotype in the Ror?-/- mice was also associated with increased bone protein levels of TCF7 and OPG. These data demonstrate that loss of Ror? has beneficial skeletal effects by increasing bone formation and decreasing bone resorption, at least in part through ?-catenin-dependent activation of the Wnt pathway. Thus, inhibition of Ror? represents a novel approach to potentially prevent or reverse osteoporosis. © 2017 American Society for Bone and Mineral Research.

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MYC Amplifies Gene Expression through Global Changes in Transcription Factor Dynamics

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Helicase-like transcription factor (Hltf) gene-deletion promotes oxidative phosphorylation (OXPHOS) in colorectal tumors of AOM/DSS-treated mice

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Proteomic analysis demonstrated transcription factor gene YRR1 deletion in Saccharomyces cerevisiae enhances its resistance to vanillin through the upregulation of transcriptional activator Haa1, coactivator Mbf1, and proteasome assembly chaperone Tma17 expression

Project description:Vanillin is one of the major phenolic inhibitors of Saccharomyces cerevisiae in lignocellulosic hydrolysates. Deleting transcription factor gene YRR1 improves vanillin resistance by promoting some translation-related processes that were confirmed at the transcription level in our previous studies. In this work, we investigated the effect of proteomic change on vanillin stress and YRR1 deletion. In wild-type cells, vanillin reduced the number of ribosomal proteins and thereby inhibited cells’ translation. YRR1 deletion increased 112 protein quantities; 48 of 112 up-regulated proteins are involved in the stress response, translational and basal transcriptional regulation. Fermentation data showed that the overexpression of HAA1, MBF1, and TMA17, which encode transcriptional activator, coactivator, and proteasome assembly chaperone, respectively, enhanced resistance to vanillin in S. cerevisiae. These results enriched the perspective of molecular mechanisms for YRR1 deletion to protect yeast from vanillin stress and offered novel targets for designing inhibitor-resistant ethanologenic yeast strains.

2021-09-09 | PXD017738 | Pride

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