RNAseq in LSD1 mouse stem cell models
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq X
ORGANISM(S): Mus musculus
SUBMITTER:
PROVIDER: E-MTAB-14221 | biostudies-arrayexpress |
SECONDARY ACCESSION(S): ERP161689
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Lysine-specific demethylase 1 (LSD1) is a histone demethylase that promotes stemness and cancer cell survival, including in prostate cancer. Most prostate malignancies are adenocarcinomas with luminal differentiation. However, a subset of tumors undergoes cellular reprogramming to a more lethal neuroendocrine prostate cancer (NEPC) with neuronal differentiation. The frequency of NEPC is increasing since widespread use of potent androgen receptor signaling inhibitors. Currently, there are no effective treatments for NEPC. We previously determined that LSD1 promotes survival of prostate adenocarcinoma tumors. However, role of LSD1 in NEPC is largely unknown. We sought to identify key genes and molecular pathways controlled by LSD1 in NEPC. We therefore inhibited LSD1 with SP2509 and performed RNA-seq in LASCPC-01, LNCaP-N-Myc, and MR42D cell lines. The vast majority of differentially expressed genes after SP2509 treatment were upregulated, suggesting that LSD1 may primarily function as a transcriptional repressor in NEPC. RNA-seq analysis reveals that LSD1 represses pathways linked to luminal differentiation and TP53 is the top pathway reactivated after LSD1 suppression. Taken together, these data suggest that LSD1 may be an important regulator of TP53 function in prostate cancer.
2023-08-30 | GSE218993 | GEO
Project description:An observational experiment to RNA-seq profile 331 primary tumours from patients diagnosed with Medulloblastoma.
2022-09-01 | E-MTAB-10767 | biostudies-arrayexpress
Project description:We report the identification of LSD1 binding genomic regions in mouse embryonic stem cells (ESC) by high throughput sequencing. By obtaining over 10 million 36 bp reads of sequence from each chromatin immunoprecipitated DNA, we generated genome-wide maps for LSD1 and histone H3 dimethylated on lysine 4 (H3K4me2), the substrate for LSD1 in mouse ESCs. Our results showed an extensive overlap between the LSD1 and H3K4me2 genomic regions and a correlation between the genomic levels of LSD1/H3K4me2 and gene expression, including many highly expressed ESC genes. LSD1 is recruited to the chromatin of cells in the G1/S/G2 phases and is displaced from the chromatin of M phase cells, suggesting that LSD1 or H3K4me2 alternatively occupies LSD1 genomic regions during cell cycle progression. LSD1 knockdown by RNA interference or its displacement from the chromatin by anti-neoplastic agents caused an increase in the levels of a subset of LSD1 target genes. Taken together, these results suggest that cell-cycle dependent association and dissociation of LSD1 with chromatin mediates short-time scale gene expression changes during ES cell cycle progression. Examination of LSD1 and lysine 4 dimethylated histone H3 (H3K4me2) binding genomic regions in embryonic stem cells. Input genomic DNA and DNA immunoprecipitaed with control IgG was included as controls.
2012-10-03 | E-GEOD-18515 | biostudies-arrayexpress
Project description:This experiment seeks to elucidate the functional role of MYB73 in Arabidopsis thaliana siliques via differential gene expression (DGE) analysis. Total RNA were extracted from pooled Arabidopsis siliques at 12 days after flowering (DAF) for 3 biological replicates from WT and MYB73-OE lines. RNA-seq libraries were generated using NEBNext Ultra II Directional RNA Library Prep Kit (New England Biolabs) for Illumina according to the manufacturer’s instruction and sequenced with Novaseq-6000 (Illumina) using paired-end sequencing with read lengths of 150 base pairs at sequencing depths of ~ 2 million reads per sample.
2024-11-01 | E-MTAB-14541 | biostudies-arrayexpress
Project description:This experiment seeks to elucidate the functional role of the ZFP2 transcription factor in Arabidopsis thaliana siliques via differential gene expression analysis. Total RNA extracted from pooled Arabidopsis siliques 12 days after flowering (DAF) was used for the assay, with 3 biological replicates each for WT and zfp2-2. For each sample, RNA-seq libraries were generated using NEBNext Ultra II Directional RNA Library Prep Kit for Illumina and sequenced with Illumina Novaseq-6000 using paired-end sequencing with read lengths of 150 base pairs at sequencing depths of ~ 2 million reads per sample.
2024-11-30 | E-MTAB-14605 | biostudies-arrayexpress
Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We dissociated crypts into single cells, and FACS sorted Epcam+ cells, to avoid immune-cell contamination. RNA was directly isolated from these sorted cells, and this was used for RNA seq. As KO crypts are different from WT crypts (KO crypts lack Paneth cells), identifying genes specifically regulated by LSD1 helps us to identify how LSD1 regulates intestinal crypt biology. Specifically, because we were able to combine this with ChIP-seq of the same cells, to identify where H3K4me1 levels (target of the histone demethylase LSD1) were different in the genome.
2020-11-16 | E-MTAB-7862 | biostudies-arrayexpress
Project description:Lsd1 ablation triggers metabolic reprogramming of brown adipose tissue. Lsd1 protein complexes were purified from mouse adipose tissue and analyzed by label-free LC-MS/MS. Mice were kept under different conditions prior complex isolation.
2017-01-03 | PXD004745 | Pride
Project description:Here we describe that lysine-specific demethylase 1 (Lsd1/KDM1a), which demethylates histone H3 on LysM-bM-^@M-^I4 or LysM-bM-^@M-^I9 (H3K4/K9), is an indispensible epigenetic governor of hematopoietic differentiation. Integrative genomic analysis in primary hematopoietic cells, combining global occupancy of Lsd1, genome-wide analysis of its histone substrates H3K4 mono- and di-methylation and gene expression profiling, reveals that Lsd1 represses hematopoietic stem and progenitor cell (HSPC) gene expression programs during hematopoietic differentiation. We found that Lsd1 function was not restricted to transcription start sites, but is also critical at enhancers. Loss of Lsd1 at these sites was associated with increased H3K4me1 and H3K4me2 methylation levels on HSPC genes and their derepression. Failure to fully silence HSPC genes compromised differentiation of hematopoietic stem cells and mature blood cell lineages. Our data indicate that Lsd1-mediated concurrent repression of enhancer and promoter activity of stem and progenitor cell genes is a pivotal epigenetic mechanism required for proper hematopoietic maturation. To identify direct target genes of Lsd1 in myeloid cells we mapped global occupancy of Lsd1 in 32D granuolocytic progenitor cells and compared H3K4me1/me2/me3 and H3K27ac histone modifications in Lsd1fl/fl (wild type) vs. Lsd1fl/f Mx1Cre (knockout) Gr1dim Mac1 granuolocytic progenitor cells.
2013-06-25 | E-GEOD-40440 | biostudies-arrayexpress
Project description:LSD1 (also known as KDM1A) is a histone demethylase and a key regulator of gene expression in embryonic stem cells and cancer.1,2 LSD1 was initially identified as a transcriptional repressor via its demethylation of active histone H3 marks (di-methyl lysine 4 [2MK4]).1 In prostate cancer, specifically, LSD1 also co-localizes with the AR and demethylates repressive 2MK9 histone marks from androgen-responsive AR target genes, facilitating androgen-mediated induction of AR-regulated gene expression and androgen-induced proliferation in androgen-dependent cancers. We report here that the LSD1 protein is universally upregulated in human CRPC and promotes survival of CRPC cell lines. This effect is explained in part by LSD1-induced activation of cell cycle and embryonic stem cell gene setsâgene sets enriched in transcriptomal studies of lethal human tumors. Importantly, despite the fact that many of these genes are direct LSD1 targets, we did not observe histone methylation changes at the LSD1-bound regions, demonstrating non-canonical histone demethylation-independent mechanisms of gene regulation. This ChIP-seq dataset included H3K4me2 and H3K9me2 ChIP-seq data for siRNA target against LSD1 and non-targeting control, as well as SP2509 inhibition of LSD1 and mock treatment 4 conditions: siRNA against LSD1, siRNA against luciferase (non-targeting control); SP2509 inhibition of LSD1, mock treatment. There are 2 replicates per condition.
2016-06-30 | E-GEOD-77762 | biostudies-arrayexpress
Project description:LSD1 inhibtion in NEPC cell line models.
| PRJNA906527 | ENA