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Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Pax6]

ABSTRACT: Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Pax6]

PROVIDER: PRJNA496335 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8053140_1.fastq.gz	Fastqsanger.gz
	SRR8053140_2.fastq.gz	Fastqsanger.gz
	SRR8053141_1.fastq.gz	Fastqsanger.gz
	SRR8053141_2.fastq.gz	Fastqsanger.gz
	SRR8053142_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Dlx1/2 Are Central and Essential Components in the Transcriptional Code for Generating Olfactory Bulb Interneurons

Project description:Generation of olfactory bulb (OB) interneurons requires neural stem/progenitor cell specification, proliferation, differentiation, and young interneuron migration and maturation. Here, we show that the homeobox transcription factors Dlx1/2 are central and essential components in the transcriptional code for generating OB interneurons. In Dlx1/2 constitutive null mutants, the differentiation of GSX2+ and ASCL1+ neural stem/progenitor cells in the dorsal lateral ganglionic eminence is blocked, resulting in a failure of OB interneuron generation. In Dlx1/2 conditional mutants (hGFAP-Cre; Dlx1/2F/- mice), GSX2+ and ASCL1+ neural stem/progenitor cells in the postnatal subventricular zone also fail to differentiate into OB interneurons. In contrast, overexpression of Dlx1&2 in embryonic mouse cortex led to ectopic production of OB-like interneurons that expressed Gad1, Sp8, Sp9, Arx, Pbx3, Etv1, Tshz1 and Prokr2. Pax6 mutants generate cortical ectopia with OB-like interneurons, but do not do so in compound Pax6; Dlx1/2 mutants. We propose that DLX1/2 promote OB interneuron development mainly through activating the expression of Sp8/9, which further promote Tshz1 and Prokr2 expression. Based on this study, in combination with earlier ones, we propose a transcriptional network for the process of OB interneuron development. This SuperSeries is composed of the SubSeries listed below.

2019-01-24 | GSE121215 | GEO

Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Dlx1/2]

Project description:Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Dlx1/2]

| PRJNA496340 | ENA

Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Pax6]

Project description:Purpose: To assess changes in gene expression profiles from the E16.5 wild type littermate controls cortex and Pax6 sey/sey mutant mice cortex. Methods: Total RNA was isolated and sequenced using an Illumina Hi-seq 2500. Raw data was analyzed using TopHat. Genes were considered significantly changed which perform P value <= 0.05. Results: Compared to controls, 173 genes were significantly down regulated, and 245 genes were up regulated in the RNA expression level of the mutant cortex.

2019-01-25 | GSE121213 | GEO

Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Dlx1/2]

Project description:Purpose: To assess changes in gene expression profiles from the E16.5 wild type littermate controls LGE and Dlx1/2-/- mutant mice LGE (lateral ganglionic eminence). Methods: Total RNA was isolated and sequenced using an Illumina Hi-seq 2500. Raw data was analyzed using TopHat. Genes were considered significantly changed which perform fold-change>=2 and P value <= 0.05. Results: Compared to controls, 804 genes were significantly down regulated, and 673 genes were up regulated in the RNA expression level of the mutant LGE.

2019-01-25 | GSE121214 | GEO

Dlx1/2 Are Central and Essential Components in the Transcriptional Code for Generating Olfactory Bulb Interneurons

Project description:Dlx1/2 Are Central and Essential Components in the Transcriptional Code for Generating Olfactory Bulb Interneurons

| PRJNA496339 | ENA

NOTCH, ERK and SHH signaling respectively control the fate determination of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons

Project description:During cortical development, radial glial cells, known as neural stem cells, initially generate a large number of cortical glutamatergic pyramidal neurons through a process called neurogenesis. This is followed by the generation of a diversity of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons, known as gliogenesis. However, the molecular mechanisms underlying the switch from cortical neurogenesis to gliogenesis, and the subsequent fate determination of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons, remain unclear. Here, we report that extracellular signal-regulated kinase (ERK) signaling plays a fundamental role in promoting cortical gliogenesis and the generation of cortical glial progenitors. Additionally, SHH-SMO-GLI activator signaling has an auxiliary function to ERK during these processes. We further demonstrate that NOTCH signaling is absolutely required for the fate determination of astrocytes, while ERK signaling plays a prominent role in oligodendrocyte fate specification, and SHH signaling is crucial for the fate determination of olfactory bulb interneurons from cortical progenitors. We provide evidence suggesting that this mechanism is conserved in both mice and humans. Finally, we propose a unifying principle of mammalian cortical gliogenesis.

2024-08-23 | GSE274547 | GEO

NOTCH, ERK and SHH signaling respectively control the fate determination of cortical astrocytes, oligodendrocytes, and olfactory bulb interneurons [CUT&Tag]

2024-08-21 | GSE275004 | GEO

Dlx1/2 are Central and Essential Components in the Transcriptional Code for Generating Olfactory Bulb Interneurons.

Project description:Generation of olfactory bulb (OB) interneurons requires neural stem/progenitor cell specification, proliferation, differentiation, and young interneuron migration and maturation. Here, we show that the homeobox transcription factors Dlx1/2 are central and essential components in the transcriptional code for generating OB interneurons. In Dlx1/2 constitutive null mutants, the differentiation of GSX2+ and ASCL1+ neural stem/progenitor cells in the dorsal lateral ganglionic eminence is blocked, resulting in a failure of OB interneuron generation. In Dlx1/2 conditional mutants (hGFAP-Cre; Dlx1/2F/- mice), GSX2+ and ASCL1+ neural stem/progenitor cells in the postnatal subventricular zone also fail to differentiate into OB interneurons. In contrast, overexpression of Dlx1&2 in embryonic mouse cortex led to ectopic production of OB-like interneurons that expressed Gad1, Sp8, Sp9, Arx, Pbx3, Etv1, Tshz1, and Prokr2. Pax6 mutants generate cortical ectopia with OB-like interneurons, but do not do so in compound Pax6; Dlx1/2 mutants. We propose that DLX1/2 promote OB interneuron development mainly through activating the expression of Sp8/9, which further promote Tshz1 and Prokr2 expression. Based on this study, in combination with earlier ones, we propose a transcriptional network for the process of OB interneuron development.

| S-EPMC6917526 | biostudies-literature

DLX1 and the NuRD complex cooperate in enhancer decommissioning and transcriptional repression

Project description:In the developing subpallium, the fate decision between neurons and glia is driven by expression of Dlx1/2 or Olig1/2 respectively, two sets of transcription factors (TFs) with a mutually repressive relationship. The mechanism by which Dlx1/2 repress progenitor and oligodendrocyte fate, while promoting transcription of genes needed for differentiation, is not fully understood. We identified a motif within DLX1 that binds RBBP4, a NuRD complex subunit. ChIP-seq studies of genomic occupancy of DLX1 and six different members of the NuRD complex show that DLX1 and NuRD colocalize to putative regulatory elements (pREs) enriched near other transcription factor genes. Loss of Dlx1/2 leads to dysregulation of genome accessibility at pREs near genes repressed by Dlx1/2, including Olig2. Consequently, heterozygosity of Dlx1/2 and Rbbp4 leads to an increase in the production of OLIG2+ cells. These findings highlight the importance of the interplay between TFs and chromatin remodelers in regulating cell fate decisions.

2022-06-01 | GSE194076 | GEO

Transcription profiling of embryonic basal ganglia and cortex in wild type and Dlx1/2 mutant mice to identify genes that are downstream of Dlx1/2 functions

Project description:The Dlx homeodomain transcription factors are implicated in regulating the function of inhibitory neurons; therefore understanding their functions will provide insights into disorders such as epilepsy, mental retardation, autism and cerebral palsy. Comparing gene expression in the embryonic basal ganglia and cortex in wild type and dlx1/2 mutant mice will provide information regarding the types of genes that are downstream of Dlx1/2 function. Perform gene array analyses in duplicate or triplicate; compare expression profile of total RNA from wild type and dlx1/2 telencephalons. I am sending separate samples of the Basal Ganglia (BG) and cortex. I want to perform gene expression comparison between: 1) wild type and dlx1/2 basal ganglia (BG) 2) wild typee and dlx1/2 cortex (ctx). Age of all mice has been indicated as 14 days to satisfy system requirements, however all mice are embryonic day 14.5.

2007-09-21 | E-GEOD-2161 | biostudies-arrayexpress

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