Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA106661 | ENA |
REPOSITORIES: ENA
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Project description:This experiment studies the gene expression in the mature olfactory sensory neurons and the intermidiate neuronal progenitors in the olfactory epithelia during the critical period. Mature olfactory sensory neurons from OMP-GFP mice and intermediate neuronal progenitors in the olfactory epithelia from Neurog1-GFP mice were FACS purified. PolyA RNA profiles at P2, P3, P7, P9, and P16 were generated by RNA-Seq.
2022-08-29 | GSE147460 | GEO
Project description:Cortical development is a complex process involving the generation of neuronal progenitors, which proliferate and migrate to form the stratified layers of the maturing cortex. To identify microRNAs (miRNAs) and genes that may be important during early cortical development, we analyzed the expression profiles of rat neuronal progenitors obtained at embryonic day 11 (E11), E12 and E13 using microarrays. Neuronal progenitors were purified from telencephalic dissociates with a positive-selection strategy using surface labeling tetanus-toxin and cholera-toxin and fluorescence-activated cell sorting. We identified classes of miRNAs and mRNAs that were up-regulated or down-regulated in these neuronal progenitors as cortical development progressed from E11 to E13. We present data that supports a regulatory role for miRNAs during the transition from neuronal progenitors into differentiating cortical neurons. Experiment Overall Design: Flow cytometry was used to isolate tetanus toxin+ and cholera toxin+ neuronal progenitors from embryonic days 11, 12 and 13 rat telencephalon. 4 biological replicates were obtained for each group using a pooled litters for each biological replicate on different prepararation days
2009-01-13 | E-GEOD-11334 | biostudies-arrayexpress
Project description:Genome-wide mRNA expression profiles of FACS-purified rat beta cells freshly isolated from control and 24h-fasted rats
| PRJNA146225 | ENA
Project description:Cortical development is a complex process involving the generation of neuronal progenitors, which proliferate and migrate to form the stratified layers of the maturing cortex. To identify microRNAs (miRNAs) and genes that may be important during early cortical development, we analyzed the expression profiles of rat neuronal progenitors obtained at embryonic day 11 (E11), E12 and E13 using microarrays. Neuronal progenitors were purified from telencephalic dissociates with a positive-selection strategy using surface labeling tetanus-toxin and cholera-toxin and fluorescence-activated cell sorting. We identified classes of miRNAs and mRNAs that were up-regulated or down-regulated in these neuronal progenitors as cortical development progressed from E11 to E13. We present data that supports a regulatory role for miRNAs during the transition from neuronal progenitors into differentiating cortical neurons. Keywords: Developmental
2008-12-01 | GSE11334 | GEO
Project description:During cortical development neurons are generated sequentially from basal progenitors (BPs) which specifically express the transcription factor Tbr2. We used fluorescent-activaed cell sorting (FACS) to isolate BPs from Tbr2GFP knockin reporter mice (Arnold SJ et al. Genesis, 2009) at early (embryonic day, E13) and late (embryonic day, E16) stages of cortical neurogenesis and determined miRNA expression profiles using mouse miRNA microarray (Agilent).Comparison of E13 and E16 microRNA expression profiles allowed us to identify regulatory mechanisms for maintaining stage specific homeostasis of BPs. FACS isolated BPs at E13 and E16 mouse brain cortex were used for miRNA microarray analyses. Four biological replicates (embryonic cortex from three different litters) for each group (E13 or E16) were analysed.
2014-05-01 | E-GEOD-45449 | biostudies-arrayexpress
Project description:The RE1 Silencing Transcription Factor (REST) in stem cells represses hundreds of genes essential to neuronal function. During neurogenesis, REST is degraded in neural progenitors to promote subsequent elaboration of a mature neuronal phenotype. Prior studies indicate that part of the degradation mechanism involves phosphorylation of two sites in the C-terminus of REST that require activity of the E3 ubiquitin ligase, bTrCP. We identify a new proline-directed phosphorylation motif, at Serines 861/864 upstream of these sites, which is a substrate for the Peptidyl-prolyl cis-trans Isomerase, Pin1, as well as the ERK1/2 kinases. Mutation at S861/864 stabilizes REST, as does inhibition of Pin1 activity. Interestingly, we find that C-Terminal Domain Small Phosphatase1 (CTDSP1) is recruited by REST to neuronal genes, is present in REST immunocomplexes, dephosphorylates S861/864 and stabilizes REST. Expression of a REST peptide containing S861/864 in neural progenitors inhibits terminal neuronal differentiation. Together with previous work indicating that both REST and CTDSP1 are expressed to high levels in stem cells and down regulated during neurogenesis, our results suggest that CTDSP1 activity stabilizes REST in stem cells, and that ERK dependent phosphorylation combined with Pin1 activity promotes REST degradation in neural progenitors.
2014-09-15 | PXD001127 | Pride
Project description:Neuronal restricted progenitors (NRPs) represent a type of transitional intermediate cells that lie between multipotent neural progenitors (NPs) and terminal differentiated neurons during neurogenesis. These NRPs have the ability to self-renew and differentiate into neurons, but not into glial cells, which is considered as an advantage for cellular therapy of human neurodegenerative diseases. However, difficulty in the extraction of highly purified NPRs from normal nervous tissue prevents further studies and applications. In this study, we reported conversion of human fetal dermal fibroblasts into human induced neuronal restricted progenitors (hiNRPs) in seven days by using just three defined factors: Sox2, c-Myc, and either Brn2 or Brn4. The hiNRPs exhibited distinct neuronal characteristics, including cell morphology, multiple neuronal markers expression, self-renewal capacity, and genome-wide transcriptional profile. Moreover, hiNRPs were able to differentiate into various terminal neurons with functional membrane properties, but not glial cells. Direct generation of hiNRPs from somatic cells will provide a new source of cells for cellular replacement therapy of human neurodegenerative diseases. This is a general expression microarray design (NimbleGen platform). It includes 5 samples.
2013-10-24 | E-GEOD-51580 | biostudies-arrayexpress
Project description:A switch from neuronal network development to maintenance during postnatal development of rat prefrontal cortex
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Project description:Non-coding RNAs regulate many biological processes including neurogenesis. The brain-enriched miR-124 is assigned as a key player of neuronal differentiation via its complex, but little understood, regulation of thousands of annotated targets. To systematically chart its regulatory functions, we used CRISPR/Cas9 gene editing to disrupt all six miR-124 alleles in human stem cells. Upon neuronal induction, miR-124-depleted cells underwent neurogenesis and became functional neurons, albeit with altered morphology and neurotransmitter specification. By RNA-induced-silencing-complex precipitation, we found that other miRNA species were upregulated in miR-124 depleted neurons. Furthermore, we identified 98 miR-124 targets of which some directly led to decreased viability. We performed advanced transcription-factor-network analysis and revealed indirect miR-124 effects on apoptosis and neuronal subtype differentiation. Our data emphasizes the need for combined experimental- and systems-level analyses to comprehensively disentangle and reveal miRNA functions, including their involvement in the neurogenesis of diverse neuronal cell types found in the human brain.
2018-10-08 | GSE118310 | GEO
Project description:Non-coding RNAs regulate many biological processes including neurogenesis. The brain-enriched miR-124 is assigned as a key player of neuronal differentiation via its complex, but little understood, regulation of thousands of annotated targets. To systematically chart its regulatory functions, we used CRISPR/Cas9 gene editing to disrupt all six miR-124 alleles in human stem cells. Upon neuronal induction, miR-124-depleted cells underwent neurogenesis and became functional neurons, albeit with altered morphology and neurotransmitter specification. By RNA-induced-silencing-complex precipitation, we found that other miRNA species were upregulated in miR-124 depleted neurons. Furthermore, we identified 98 miR-124 targets of which some directly led to decreased viability. We performed advanced transcription-factor-network analysis and revealed indirect miR-124 effects on apoptosis and neuronal subtype differentiation. Our data emphasizes the need for combined experimental- and systems-level analyses to comprehensively disentangle and reveal miRNA functions, including their involvement in the neurogenesis of diverse neuronal cell types found in the human brain.
2018-10-08 | GSE118307 | GEO