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ABSTRACT: RNA-seq for T3 treatment of Sertoli cells

PROVIDER: PRJNA1040123 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26864054_1.fastq.gz	Fastqsanger.gz
	SRR26864054_2.fastq.gz	Fastqsanger.gz
	SRR26864055_1.fastq.gz	Fastqsanger.gz
	SRR26864055_2.fastq.gz	Fastqsanger.gz
	SRR26864056_1.fastq.gz	Fastqsanger.gz

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Project description:RNA-seq for T3

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Thyroid hormone-mediated histone modificaiton protects primary mouse cortical neurons from the toxic effects of hypoxic injury.

Project description:Epigenetic and genetic regulation mediates the response to stress at the cellular level and allows cells for adaptation and survival. Thyroid hormone has been shown to have a protective role in neuronal injury, although the mechanisms are not established. We hypothesized that the neuroprotective role of thyroid hormone was associated with epigenetic modifications of histone proteins. We used hypoxic neurons as a model system for hypoxia-induced brain injury. Mouse primary cortical neurons were exposed to 0.2% oxygen for 7 hours with or without treatment with 10 nM Triiodotyroxine (T3). We analyzed the mRNA expression of histone modifying enzymes by RNA-seq and the posttranslationally modified histone 3 proteins by ELISA assay and Western blot. We found that methylation of H3K27, associated with inactive promoters, was highly induced in hypoxic neurons, and this methylation was reduced by T3 treatment. H3K4 methylation is the hallmark of active promoters. Three (Set1db, Kmta2c and Kmt2e) out of six H3K4 methyltransferases were downregulated by hypoxia and restored by T3 treatment. H3K4me3 protein, by ELISA assay, was increased 76% in T3-treated hypoxic neurons, compared to without T3 treatment. H3K56ac, plays a critical role in transcription initiation, was markedly increased in T3-treaed hypoxic neurons, compared to those without T3 treatment, indicating that T3 treatment stimulated gene transcription. Additionally, T3 treatment restored hypoxia-induced downregulation of histone acetyltransferase, Kat6a, Kat6b and Crebbp, which function as transcription factors. These findings indicate that T3 treatment mitigates hypoxia-induced alteration of the histone modifications and protects neurons from hypoxia-induced injury.

2022-07-27 | GSE205801 | GEO

Identification of a novel transcriptional variant in the mouse Sry locus by long-read RNA-seq and conventional RNA-seq

Project description:The mammalian sex-determining gene Sry induces male development. Sry is exclusively expressed in Nr5a1-highly expressing gonadal supporting cell precursor, pre-Sertoli cells, with a peak at embryonic day 11.5 (E11.5). We developed a method to enrich pre-Sertoli cells from mouse embryonic gonads carrying Nr5a1-hCD271 (LNGFR) transgene. To examine mRNA expression in pre-Sertoli cells, pre-Sertoli cells were purified and introduced into long-read RNA-seq and conventional RNA seq analyses. Through analyzing those RNA-seq data, we discovered a second exon of mouse Sry.

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Project description:Stem cells respond to triiodothytonine (T3) treatment

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Next Generation Sequencing Facilitates Quantitative Analysis of treated and untreated mortical neurons GDE

Project description:Traumatic Brain Injury (TBI) is associated with disruption of cerebral blood flow leading to localized brain hypoxia. Thyroid hormone (TH) treatment, when administered shortly after injury, has been shown to promote neural protection in rodent TBI models. The mechanism of TH protection, however, is not established. We used mouse primary cortical neurons to investigate the effectiveness and mechanism of T3-promoted cell survival after exposure to hypoxic injury. Cultured primary cortical neurons were exposed to hypoxia (0.2% oxygen) for 7 hours, in either the presence or absence of T3 (5 nM). T3 treatment enhanced DNA 5-hydroxymethylcytosin (5-hmc) levels and attenuated the hypoxia-induced increase in DNA 5-methylcytosin (5-mc). In the presence of T3, mRNA expression of Tet family genes was increased and DNA methyltransferases, (Dnmt) 3a and Dnmt3b, were downregulated, compared to conditions in the absence of T3. These T3-induced changes decreased hypoxia-induced DNA de novo methylation, which reduced hypoxia-induced neuronal damage and apoptosis. We utilized RNA-seq to characterize T3-regulated genes in cortical neurons under hypoxic conditions and identified 22 genes that were upregulated and 15 genes that were downregulated. Krupple-like factor 9 (KLF9), a multifunctional transcription factor that plays a key role in CNS development, was highly upregulated by T3 treatment in hypoxic conditions. Knockdown of the KLF9 gene resulted in early apoptosis and abolished the beneficial role of T3 in neuronal survival. KLF9 mediates, in part, the neuronal protective role of T3. T3 treatment reduces hypoxic damage and acts through pathways that reduce DNA methylation and apoptosis.

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Polycomb suppresses a female gene regulatory network in Sertoli cells

Project description:To examine the function of PRC1 in postnatal Sertoli cells, we performed RNA-seq using PRC1 conditional KO and control mouse Sertoli cells. We also analyzed the distribution of H2AK119ub, H3K27me3 and RNF2 by ChIP-seq.

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2021-06-09 | GSE167909 | GEO

To evaluate the change in gene expression profile of Sertoli cells after busulphan treatment

Project description:In order to evaluate whether chemoablative busulphan treatment alters the expression profile of Sertoli cells in testis, adult male Swiss mice were treated intraperitoneally with 25mg/Kg body weight of busulphan. 1 month post busulphan treatment, the isolated Sertoli cells were evaluated for gene expression profile and compared to expression profile of Sertoli cells from age matched normal adult Swiss mice.

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Functional definition of thyroid hormone response elements based on a synthetic Starr-seq screen

Project description:We performed an original protocol called synthetic STARR-seq (PMID: 30427832) in which a library of putative response elements are tested for their capacity to bind thyroid hormone (T3) nuclear receptors and convey T3 transactivation More than 10 000 putative T3 response elements (T3RE) were cloned in the hSTARR-seq-ORI vector with a minimal promoter, in the 3' end of the transcribed sequence. These are variant of the consensus T3RE (5'NGGTCANNNNRGGNNA3') Therefore the most active T3RE are over-represented in the RNA of cells transfected with the plasmid library and treated with T3.

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