Identification of Klf9-regulated genes in HT22 tissue culture cells
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PROVIDER: PRJNA343879 | ENA |
REPOSITORIES: ENA
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Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration. We used mouse hippocampus-derived HT22 cell line to identify genes differentially regulated by forced Klf9 expression. We stably transfected HT22 cells with pCDNA6:TR (encoding the Tet repressor) and pCDNA6:TO-Klf9 (encoding Klf9 downstream of the Tet operator), allowing doxycycline(dox)-inducible expression of Klf9. We chose a stably transfected clone with baseline Klf9 mRNA level similar to that of untransfected HT22 cells (parent line) and approximately 10-fold induction after dox treatment. We conducted RNA-seq on stably transfected HT22 cells treated with or without dox for 8 hours; we also conducted RNA-seq on parent cells subjected to the same dox treatment to separate nonspecific effects of dox from the effects of forced Klf9 expression. Analysis of RNA-seq data found 217 gene repressed and 21 upregulated by forced Klf9 expression (FDR-adjusted p<.005; because fold changes were small we used a stringent p value cutoff to ensure that we were studying genes likely to be bona fide targets), showing that Klf9 functions primarily as a transcriptional repressor. Gene ontology analysis showed that Klf9-repressed genes were enriched in cytoskeletal and Wnt signaling-related genes.
2019-09-19 | GSE87093 | GEO
Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration, but none of its genomic targets are known in neurons. We used the mouse hippocampus-derived cell line HT22 to identify Klf9’s genomic binding sites in neurons. We stably transfected HT22 cells with the biotin ligase BirA with or without co-transfection of a Klf9 fusion protein with an n-terminal FLAG tag and a biotin ligase recognition peptide. This allowed us to precipitate Klf9 in chromatin using streptavidin. This permits the use of more stringent wash conditions, improving signal-to-noise ratio. We conducted high-throughput sequencing on DNA precipitated from these lines and identified 3,378 regions where Klf9 associated in chromatin. We found that Klf9 associated near transcription start sites and that its genomic targets were enriched for genes related to cytoskeletal regulation and apoptosis.
2019-09-19 | GSE87203 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-09-19 | GSE87206 | GEO
Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChipM-BM-. Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour. The gene expression profile from the J147-treated HT22 cells (1 hour exposure) was compared to HT22 cells treated with vehicle only (DMSO) for 1 hour. The DMSO/vehicle treated cells serve as the control and are referred to as untreated with drug.
2013-03-28 | E-GEOD-45534 | biostudies-arrayexpress
Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChip® Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour.
2013-03-28 | GSE45534 | GEO
Project description:Identification of Klf9-regulated genes in HT22 tissue culture cells [RNA-Seq]
| PRJNA343482 | ENA
Project description:A Krüppel-like factor 9 (Klf9) regulated network in HEC-1-A endometrial carcinoma cells encompassing adhesion proteins, steroid- and menstrual cycle-regulated proteins of the uterine endometrium, novel membrane proteins, and nuclear receptors
2009-06-23 | GSE11855 | GEO
Project description:The induction of beige adipocytes in white adipose tissue (WAT), also known as WAT beiging, improves glucose and lipid metabolism. However, the regulation of WAT beiging at the posttranscriptional level remains elusive. Here, we report that METTL3, the methyltransferase of N6-methyladenosine (m6A) mRNA modification, is induced during WAT beiging in mice. Adipose-specific depletion of Mettl3 gene undermines WAT beiging. Transcriptomic analysis of m6A modifications and mRNA expression level reveals global reduction of m6A-modified mRNAs in Mettl3-depleted beige adipose tissue. In particular, METTL3-catalyzed m6A installation on Krüppel-like factor 9 (Klf9) mRNA prevents its degradation. We further demonstrate that the m6A reader protein IGF2BP3 mediates the stabilization of m6A-modified Klf9 mRNA. Overexpressioin of KLF9 protein reverses the impaired WAT beiging elicited by Mettl3 deletion. These findings uncover a novel epitranscriptional mechanism in WAT beiging and identify METTL3-KLF9 axis as a potential therapeutic target for obesity-associated disorders.
2023-02-03 | GSE178884 | GEO
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
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