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Chronic dietary exposure to the food preservative tert-Butylhydroquinone (tBHQ) impairs zebrafish (Danio rerio) survival, growth, organ development, and gene expression in Nrf2a-dependent and independent ways

ABSTRACT: Chronic dietary exposure to the food preservative tert-Butylhydroquinone (tBHQ) impairs zebrafish (Danio rerio) survival, growth, organ development, and gene expression in Nrf2a-dependent and independent ways

PROVIDER: PRJNA911635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22705101_1.fastq.gz	Fastqsanger.gz
	SRR22705101_2.fastq.gz	Fastqsanger.gz
	SRR22705102_1.fastq.gz	Fastqsanger.gz
	SRR22705102_2.fastq.gz	Fastqsanger.gz
	SRR22705103_1.fastq.gz	Fastqsanger.gz

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Chronic dietary exposure to the food preservative tert-Butylhydroquinone (tBHQ) impairs zebrafish (Danio rerio) survival, growth, organ development, and gene expression in Nrf2a-dependent and independent ways

Project description:Tert-Butylhydroquinone (tBHQ), a preservative used to prevent oxidative deterioration of oil, fat, and meat products, has been linked to both chemoprotective and adverse effects. This study investigates the impact of chronic dietary tBHQ on survival, growth parameters, organ development, and gene expression in zebrafish (Danio rerio). As tBHQ activates the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2a), a zebrafish line with a mutation in the DNA-binding domain was used to identify Nrf2a-dependent vs. independent effects. Homozygous Nrf2a wildtype (wt) and mutant (m) larvae were fed a diet containing 5% tBHQ or a control diet. Survival and growth parameters were assessed at 15 days and at 5 months, and samples collected for RNA sequencing at 5 months. Chronic dietary exposure to tBHQ throughout the larval and juvenile periods negatively impacted growth and survival. RNA-seq analysis found differentially expressed genes related to growth and development and upregulation of several immune pathways. The findings herein demonstrate that chronic dietary tBHQ exposure may impair growth and survival in both Nrf2a dependent and independent manners.

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Sequencing of Danio rerio muscle from tert mutants and controls

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Sequencing of Danio rerio skin from wildtype and two tert mutant phenotypes (JenAge)

Project description:Comparison of gene expression profiles from Danio rerio skin of wiltype (AB) and homozygote/heterozygote tert mutant phenotypes (AB tert(-/-), AB tert(+/)). The RNA-seq data comprises 3 groups. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)

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PITX1 suppresses TERT transcription

Project description:Using microcell-mediated chromosome transfer (MMCT) into the mouse melanoma cell line, B16F10, we have previously found that human chromosome 5 carries a gene, or genes, that can negatively regulate TERT expression. To identify the gene responsible for the regulation of TERT transcription, we performed cDNA microarray analysis using parental B16F10 cells, telomerase negative B16F10 microcell hybrids with a human chromosome 5 (B16F10MH5), and its revertant clones (MH5R) with reactivated telomerase. Here we report the identification of PITX1, whose restoration leads to the downregulation of mouse tert (mtert) transcription, as a TERT suppressor gene. Additionally, both human TERT (hTERT) and mouse TERT (mtert) promoter activity can be suppressed by PITX1. We showed that three and one binding sites, respectively, within the hTERT and mtert promoters that express a unique conserved region are responsible for the transcriptional activation of TERT. Furthermore, we showed that PITX1 binds to the TERT promoter both in vitro and in vivo. Thus, PITX1 suppresses TERT transcription through direct binding to the TERT promoter, which ultimately regulates telomerase activity.

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PITX1 suppresses TERT transcription

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Project description:Blocking telomerase is recognized as a key anti-cancer mechanism. Unlike in stem cells, levels of telomerase catalytic subunit TERT are limiting in reconstituting telomerase activity in somatic cells. However in some cancers, Tert is transcriptionally reactivated by mutations in its promoter. Given that Tert in stem cells is driven by WT Tert promoter, if we can selectively target Tert reactivation through mutant Tert promoters we can block telomerase activity specifically in cancer cells without toxicity in stem cells. Here we report the epigenetic regulation of Tert promoter comparing WT and mutant promoters. We showed that GABPA homodimerization through long-range interaction stabilizes Gabpa to drive Tert expression. Furthermore, BRD4 specifically activates the C250T mutant promoter via dual mechanism involving GABPA, thereby setting the stage for future therapeutics.

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