Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA319371 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3419771.fastq.gz | Fastqsanger.gz | |||
| SRR3419772.fastq.gz | Fastqsanger.gz | |||
| SRR3419773.fastq.gz | Fastqsanger.gz | |||
| SRR3419774.fastq.gz | Fastqsanger.gz |
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Project description:Metazoan development depends on accurate execution of differentiation programs that allow pluripotent stem cells to adopt specific fates. Differentiation is brought about by global changes to chromatin architecture and transcriptional networks, yet whether other regulatory events support cell fate determination is less well understood. Using human embryonic stem cell and Xenopus models, we identified the vertebrate-specific ubiquitin ligase Cul3KBTBD8 as an essential regulator of neural crest specification. Cul3KBTBD8 monoubiquitylates NOLC1 and its paralog TCOF1, whose mutation underlies the craniofacial disorder Treacher Collins Syndrome that is characterized by a loss of cranial neural crest cells. Ubiquitylation of NOLC1 and TCOF1 drives formation of a platform that connects RNA polymerase I with ribosome modification enzymes, thereby altering the translational program of differentiating cells to support the generation of neural crest cells. We conclude that the dynamic regulation of ribosome function is an important feature of cell fate determination. Ribosome profiling and mRNA-Seq
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Project description:To study the function of Chd5 in neuronal differentiation, we cultured primary neural stem cells from WT and Chd5 deficient embryos.
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Project description:CHD5 is frequently deleted in neuroblastoma, and appears to be a tumor suppressor gene; however, little is known about the role of CHD5. We found CHD5 mRNA was restricted to brain; by contrast most other remodeling ATPases were broadly expressed. CHD5 protein isolated from mouse brain was associated with HDAC2, p66, MTA3 and RbAp46 in a megadalton complex. CHD5 protein was detected in several rat brain regions and appeared to be enriched in neurons. CHD5 protein was predominantly nuclear in primary rat neurons and brain sections. Microarray analysis revealed genes that were upregulated and downregulated when CHD5 was depleted from primary neurons. CHD5 depletion altered expression of neuronal genes, transcription factors, and brain-specific subunits of the SWI/SNF remodeling enzyme. Aging and Alzheimers gene sets were strongly affected by CHD5 depletion from primary neurons. Chromatin immunoprecipitation revealed CHD5 bound to these genes, suggesting the regulation was direct. Together, these results indicate that CHD5 is found in a NuRD-like multi-protein complex. CHD5 is restricted to the brain, unlike the closely related family members CHD3 and CHD4. CHD5 regulates expression of neuronal genes, cell cycle genes and remodeling genes. CHD5 is linked to regulation of aging and Alzheimer’s genes. CHD5 KD shRNA sequences were designed according to the instructions for the pLKO.1 system (Addgene). Control was as described (Sci307-1098,2005) Scramble, clone 1864 from Addgene). Virus was packaged using HEK-293T cells, pLKO.1 vector with shRNA inserts for CHD5, and the control. 48 hours after transfection of 293 cells, medium containing virus was filtered (0.45 micron), then applied for 6 hours to primary cortical neurons one day after the neurons were plated (Day 1). Medium was removed, and replaced with Neural Basal Medium, and the cells were cultured until Day 5, 9 or 12. RNA was harvested from 3 replicates of the treated primary cortical neurons at each time point. RNA was isolated using RNAeasy Kit (Qiagen), Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips. RNA was labeled using the standard Illumina protocol and Illumina TotalPrep RNA Amplification Kit (Ambion; Austin, TX, cat # IL1791) Biotin labeled cRNA was hybridized to Illumina's Sentrix Rat Ref-12 v1 Expression BeadChips.
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Project description:E2A regulates neural ectoderm fate specification in human embryonic stem cells
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Project description:Recent findings suggest that the ribosome itself modulates gene expression. However, whether ribosomes change composition across cell types to control cell fate remains unknown. To determine the magnitude of ribosome heterogeneity and its functional contribution to cell fate specification, we measured ribosomal protein abundance in actively translating ribosomes by quantitative mass spectrometry on a day-by-day basis as human embryonic stem cells differentiate in a step-wise fashion down endoderm and mesoderm lineages. We identified numerous core ribosomal proteins (RPs) as changing significantly in abundance in actively translating ribosomes during cell fate specification, including progressive decreases in ribosome incorporation for several ribosomal proteins during mesoderm differentiation. We further traced ribosome composition changes at the cytoplasmic, whole-cell, and mRNA transcript levels and identified multiple mechanisms regulating actively translating ribosome composition. These findings reveal extensive ribosomal remodeling during differentiation, suggesting that individual ribosomal components may have cell type-specific specialized translation functions.
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Project description:The chromatin remodeler CHD5 is expressed in neural tissue and is frequently deleted in aggressive neuroblastoma. Very little is known about the function of CHD5 in the nervous system or its mechanism of action. Here we report that depletion of Chd5 in the developing murine neocortex blocks neuronal differentiation and leads to an accumulation of undifferentiated progenitors. CHD5 binds a large cohort of genes and is required for facilitating the activation of neuronal genes. It also binds a cohort of Polycomb targets and is required for the maintenance of H3K27me3 on these genes. Interestingly, the chromodomains of CHD5 directly bind H3K27me3 and are required for neuronal differentiation. In the absence of CHD5, a subgroup of Polycomb-repressed genes becomes aberrantly expressed. These findings provide new insights into the regulatory role of CHD5 during neurogenesis and suggest how inactivation of this candidate tumor suppressor might contribute to neuroblastoma. Examination of genome-wide binding/occupancy of CHD5 in the SH-SY5Y cell line
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