Transcriptional profiling of sequentially generated septal neuron fates
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ABSTRACT:
PROVIDER: PRJNA766715 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description: Not available
| S-EPMC8694698 | biostudies-literature
Project description:Single cell RNA-Seq analysis of the developing septum and MGE at embryonic stages, and septum at postnatal stages
2021-09-30 | GSE184879 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE33059: Sequentially acting Sox transcription factors in neural lineage development [ChIP-seq] GSE33060: Sequentially acting Sox transcription factors in neural lineage development [RNA-seq] GSE33061: Sequentially acting Sox transcription factors in neural lineage development [microarray] Refer to individual Series
2011-11-01 | E-GEOD-33024 | biostudies-arrayexpress
Project description:Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the same factors are often used to reprogram many different donor cell types. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs but not the neuronal program during reprogramming and neurogenesis and in primary mouse neurons. The repressive function of Myt1l is mediated by recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knock-down of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar ‘many-but-one’ lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types.
2017-04-05 | GSE72121 | GEO
Project description:Ventricular septal defect (VSD) is one of the most prevalent birth defects. The pathogenesis of VSD remains unknown. to analyze the expression of AF-derived lncRNAs and their roles in VSD development, Arraystar Human LncRNA Microarray V5.0 is employed for the global profiling of human lncRNAs and protein-coding transcripts.
2022-05-27 | GSE204935 | GEO
Project description:MicroRNAs (miRNAs) regulate transcription factors and relate to ventricular septal defect (VSD) occurrence, progression and outcome. Recently, circulating miRNAs from maternal blood and amniotic fluid have been used as biomarkers for congenital heart defect (CHD) diagnosis. However, whether circulating miRNAs are associated with foetal heart tissue remains unknown. Dimethadione (DMO) induced a VSD rat model and the miRNA expression profiles of the myocardium, amniotic fluid and maternal serum were analysed. MiRNAs were differentially expressed in the myocardium, amniotic fluid or maternal serum of VSD foetal rats and might be involved in cardiomyocyte differentiation and apoptosis.
2022-06-23 | GSE194240 | GEO
Project description:Notch signaling is an evolutionarily conserved pathway for specifying binary neuronal fates, yet how it specifies different fates in different contexts remains elusive. In our accompanying paper, using the Drosophila lamina neuron types (L1-L5) as a model, we show that the primary homeodomain transcription factor (HDTF) Bsh activates secondary HDTFs Ap (L4) and Pdm3 (L5) and specifies L4/L5 neuronal fates. Here we test the hypothesis that Notch signaling enables Bsh to differentially specify L4 and L5 fates. We show asymmetric Notch signaling between newborn L4 and L5 neurons, but they are not siblings; rather, Notch signaling in L4 is due to Delta expression in adjacent L1 neurons. While Notch signaling and Bsh expression are mutually independent, Notch is necessary and sufficient for Bsh to specify L4 fate over L5. The NotchON L4, compared to NotchOFF L5, has a distinct open chromatin landscape which allows Bsh to bind distinct genomic loci, leading to L4-specific identity gene transcription. We propose a novel model in which Notch signaling is integrated with the primary HDTF activity to diversify neuron types by directly or indirectly generating a distinct open chromatin landscape that constrains the pool of genes that a primary HDTF can activate.
2023-11-12 | GSE247239 | GEO
Project description:Social interactions are critical components for the survival of mammalian biology and evolution. Dysregulation of social behavior often leads to psychopathologies such as social anxiety disorder, which is characterized by an intense fear and avoidance of social situations. Using the social fear conditioning (SFC) paradigm, we analyzed expression levels of miR-132-3p and miR-124-3p within the septum, a brain region essential for social behavior and fear, after acquisition and extinction of social fear. Functional in vivo approaches using pharmacology, functional inhibition of miR-132-3p, viral miR-132 overexpression and shRNA-mediated knockdown of miR-132-3p within oxytocin receptor positive neurons confirmed septal miR-132-3p to be involved in social fear extinction and the oxytocin-mediated reversal of social fear. Moreover, Argonaute-RNA-co-immunoprecipitation-microarray analysis and further target mRNA quantification, depicted growth differentiation factor-5 (GDF-5) to be involved in miR-132-3p-mediated regulation of social fear extinction. Local application of GDF-5 resulted in impaired social fear extinction, an effect which seems to be mediated by miR-132-3p. In summary, we show that septal miR-132-3p is functionally involved in social fear extinction learning and oxytocin-mediated reversal of social fear.
2023-11-08 | GSE211449 | GEO
Project description:To investigate the role of motor neuron autophagy in ALS, we generated mice in which the critical autophagy gene Atg7 was specifically disrupted in motor neurons (Atg7 cKO). We also bred these mice to the SOD1G93A mouse model of ALS. Then we performed RNA sequencing on lumbar spinal cords from these mice to determine how motor neuron autophagy inhibition altered gene expression.
2017-08-10 | GSE100888 | GEO
Project description:Characterization of the signaling requirements to determine primitive streak and neuroectoderm fates in mouse embryonic stem cells.
2022-01-20 | E-MTAB-10242 | biostudies-arrayexpress