Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA343881 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4289490.fastq.gz | Fastqsanger.gz | |||
| SRR4289491.fastq.gz | Fastqsanger.gz | |||
| SRR4289492.fastq.gz | Fastqsanger.gz | |||
| SRR4289493.fastq.gz | Fastqsanger.gz | |||
| SRR4289494.fastq.gz | Fastqsanger.gz |
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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, 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.
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Project description:Identification of Klf9-regulated genes in HT22 tissue culture cells [RNA-Seq]
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Project description:Identification of Klf9-regulated genes in HT22 tissue culture cells
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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.
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Project description:Krüppel-like factors (KLFs) play key roles in nervous system development and function. Several KLFs are known to promote, and then maintain neural cell differentiation. Our previous work focused on the actions of KLF9 in mouse hippocampal neurons. Here we investigated genomic targets and functions of KLF9’s paralog KLF13, with the goal of understanding how these two closely related transcription factors influence hippocampal cell function, proliferation, survival and regeneration. We engineered the adult mouse hippocampus-derived cell line HT22 to control Klf13 expression with doxycycline. We also generated HT22 Klf13 knock out cells, and we analyzed primary hippocampal cells from wild type and Klf13-/- mice. RNA sequencing showed that KLF13, like KLF9, acts predominantly as a transcriptional repressor in hippocampal neurons and can regulate other Klf genes. Pathway analysis revealed that genes regulated by KLF13 are involved in cell cycle, cell survival, cytoarchitecture regulation, among others. Chromatin-streptavidin sequencing conducted on chromatin isolated from HT22 cells expressing biotinylated KLF13 identified 9506 genomic targets; 79% were located 1 kilobase upstream of transcription start sites. Transfection-reporter assays confirmed that KLF13 can directly regulate transcriptional activity of its target genes. Comparison of the target genes of KLF9 and KLF13 found that they share some functions that were likely present in their common ancestor, but have also acquired distinct functions during evolution. Flow cytometry showed that KLF13 promotes cell cycle progression, and it protects cells from glutamate-induced excitotoxic damage. Taken together, our findings establish novel roles and molecular mechanisms for KLF13 actions in mammalian hippocampal neurons.
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Project description:Identification of Bmal1 binding sites by ChIP-seq in mouse lung tissue
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Project description:Identification of in vivo binding sites for YY2.
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Project description:Comprehensive identification of the binding sites of CLOCK in the mouse liver using ChIP-Seq
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Project description:Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation and neural development; however, the molecular basis for KLF9M-bM-^@M-^Ys diverse contextual functions remains unclear. This study focuses on the functions of KLF9 in human glioblastoma stem-like cells. We establish for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stem-like cells, and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, shows that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation, and identify KLF9-regulated molecular targets applicable to cancer therapeutics. Two cell lines were used as biological replicates. Each cell line have one KLF9 ChIP-enriched DNA sample and one input genomic DNA sample.
2014-10-10 | E-GEOD-62211 | biostudies-arrayexpress