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RNAseq measurement of cortisol induced gene expression change under knockout of Klf9

ABSTRACT: RNAseq measurement of cortisol induced gene expression change under knockout of Klf9

PROVIDER: PRJNA605203 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11039800.fastq.gz	Fastqsanger.gz
	SRR11039801.fastq.gz	Fastqsanger.gz
	SRR11039802.fastq.gz	Fastqsanger.gz
	SRR11039803.fastq.gz	Fastqsanger.gz
	SRR11039804.fastq.gz	Fastqsanger.gz

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RNAseq measurement of cortisol induced gene expression change under knockout of Klf9

Project description:We found that a frameshift deletion introduced into exon 1 of zebrafish klf9 eliminates the DNA binding domain and significantly reduces expression of the mature transcript. RNA-seq shows that klf9 is required for the pro-inflammatory transcriptomic effects of chronic cortisol treatment. klf9 is one of a core set of genes consistently found to be upregulated by chronic cortisol exposure.

2020-07-15 | GSE144885 | GEO

RNAseq measurement of cortisol induced gene expression change under knockout of glucocorticoid receptor (nr3c1)

Project description:RNAseq measurement of cortisol induced gene expression change under knockout of glucocorticoid receptor (nr3c1)

| PRJNA605204 | ENA

RNAseq measurement of cortisol induced gene expression change under knockout of glucocorticoid receptor (nr3c1)

Project description:We found that GR mediates most of the effects of the treatment, and paradoxically, that the transcriptome of cortisol-treated larvae is more like that of larvae lacking a GR than that of larvae with a GR, suggesting that the cortisol-treated larvae develop GR resistance.

2020-07-15 | GSE144884 | GEO

Real-time quantitative PCR analysis of cortisol-indeced sex change in epinephelus coioides

Project description:Cortisol was injected into the protogynous epinephelus coioides to investigate the role of this hormone on sex change. Following injection, we evaluated sex-related gene expression during the processes of cortisol-induced sex change in epinephelus coioides.

2020-01-02 | GSE142814 | GEO

Klf9 is essential for cardiac mitochondrial homeostasis

Project description:Mitochondrial dynamics and mitophagy are intimately linked physiological processes that are essential for cardiac homeostasis. Here we show that cardiac Klf9 is dysregulated in human and rodent cardiomyopathy. Young adult global Klf9-knockout mice displayed hypertrophic cardiomyopathy that was characterized by depressed systolic function, increased left ventricular mass and pulmonary congestion. Klf9 knockout led to mitochondrial disarray and fragmentation in cardiomyocytes. Biochemical analysis confirmed that mitochondrial respiratory function was impaired in Klf9-knockout cardiomyocytes, with reduced myocardial ATP levels and elevated ROS. Furthermore, cardiac-specific Klf9-deficient mice phenocopied global Klf9-knockout mice, suggesting that cardiac Klf9 is essential for mitochondrial homeostasis and heart function. Moreover, cardiac Klf9 deficiency inhibited mitophagy induced by angiotensin II (ANGII), thereby leading to accumulation of dysfunctional mitochondria and acceleration of heart failure in mice in response to ANGII treatment. In contrast, cardiac-specific Klf9 transgene improved cardiac systolic function via promoting mitophagy in mice in response to ANGII treatment. Molecular mechanism studies indicated that Klf9 knockout decreased the expression of PGC-1α and its target genes involved in mitochondrial energy metabolism. Moreover, Klf9 controlled the expression of Mfn2 by directly binding to its promoter region, thereby regulating mitochondrial dynamics and mitophagy. Finally, we performed Mfn2 rescue experiments in Klf9-CKO mice and found that AAV-mediated Mfn2 rescue in heart improved cardiac mitochondrial and systolic function in Klf9-CKO mice treated with or without ANGII. Thus, Klf9 integrates cardiac energy metabolism, mitochondrial dynamics and mitophagy. Modulating Klf9 activity may have therapeutic potential in the treatment of heart failure.

2024-10-03 | GSE278326 | GEO

Global changes in gene expression in primary keratinocytes after KLF9 overexpression

Project description:To identify putative target genes of the transcription factor Klf9 in primary keratinocytes we over-expressed Klf9 in these cells using a lentiviral delivery system. We detected several hundred genes that show differential expression levels following ectopic Klf9 expression including several genes that are involved in proliferation and cell cycle control. These results allow insights into the mechanisms by which Klf9 regulates proliferation in primary keratinocytes. Primary human neonatal foreskin keratinocytes were infected with equal viral titers of a GFP and KLF9 expression construct, respectively. Cells were harvested 2,4 and 7 days after infection and total RNA was used to perform whole genome microarray analysis.

2012-07-30 | E-GEOD-36014 | biostudies-arrayexpress

Transcription profiling of jejunums from wild type and Klf9-/- mice to investigate the involvement of Klf9 in small intestine crypt-villus cell renewal and lineage determination.

Project description:Kruppel-like factor 9 (Klf9), a zinc-finger transcription factor, is implicated in the control of cell proliferation, cell differentiation and cell fate in brain and uterus. Using Klf9 null mutant mice, we have investigated the involvement of Klf9 in small intestine crypt-villus cell renewal and lineage determination. We report the predominant expression of Klf9 gene in small intestine smooth muscle (muscularis externa). Jejunums null for Klf9 have shorter villi, reduced crypt stem/transit cell proliferation, and altered lineage determination as indicated by decreased and increased numbers of Goblet and Paneth cells, respectively. A stimulatory role for Klf9 in villus cell migration was demonstrated by BrdU labeling. Results suggest that Klf9 controls the elaboration, from small intestine smooth muscle, of molecular mediator(s) of crypt cell proliferation and lineage determination, and of villus cell migration. Experiment Overall Design: Total RNA was extracted in parallel from the jejunums of five WT and five Klf9-/- male mice (PND 30) using TRIzol reagent (Invitrogen, Carlsbad, CA). Conversion of each RNA preparation to corresponding fragmented cRNA. Fifteen ug of each cRNA was hybridized for 16 hours to an Affymetrix mouse 430A GeneChip. Ten GeneChips (each corresponding to a single animal) were hybridized, washed and scanned in parallel. Following the wash, signal amplification, and signal detection steps, GeneChips were scanned (Agilent GeneArray laser scanner) and the resultant images quantified using Affymetrix MAS 5.0 software.

2007-11-15 | E-GEOD-6443 | biostudies-arrayexpress

Bulk RNA-seq of zebrafish 5dpf embryos comparing Klf9 knockout with matched controls at 3 timepoints flanking zeitgeber (lights on)

Project description:Krüppel-like factor 9 (Klf9) is a ubiquitously expressed transcription factor that is a feedforward regulator of multiple stress-responsive and endocrine signaling pathways. We previously described how loss of Klf9 function affects the transcriptome of zebrafish larvae sampled at a single time point 5 days post-fertilization (dpf). However, klf9 expression oscillates diurnally, and the time point that was sampled corresponded to its expression nadir. To determine if klf9-/- function varies with time of day, we performed bulk RNA-seq on 5 dpf zebrafish embryos sampled at three timepoints encompassing the predawn peak and midmorning nadir of klf9 expression. We found that while the major effects of the klf9-/- mutation that we reported previously are robust to time of day, the mutation has additional effects that manifest only at the predawn time point. We used a published single-cell atlas of zebrafish development to map the effects of the klf9-/- mutation onto different cell types and found that the mutation increased representation of genes associated with digestive organs (liver, pancreas, and intestine) and decreased representation of genes associated with differentiating neurons, blood, and somites. Measurements from confocally-imaged larvae suggest that overrepresentation of liver genes in klf9-/- mutants is due to development of enlarged livers.

2023-02-01 | GSE218687 | GEO

Real-time quantitative PCR analysis of cortisol-indeced sex change in epinephelus coioides

Project description:Real-time quantitative PCR analysis of cortisol-indeced sex change in epinephelus coioides

| PRJNA598445 | ENA

Global changes in gene expression in primary keratinocytes after KLF9 overexpression

2012-07-31 | GSE36014 | GEO