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Transcription factors Bcl11a and Bcl11b are Required for the production and differentiation of cortical projection neurons

ABSTRACT: Transcription factors Bcl11a and Bcl11b are Required for the production and differentiation of cortical projection neurons

PROVIDER: PRJNA758686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15663503_1.fastq.gz	Fastqsanger.gz
	SRR15663503_2.fastq.gz	Fastqsanger.gz
	SRR15663504_1.fastq.gz	Fastqsanger.gz
	SRR15663504_2.fastq.gz	Fastqsanger.gz
	SRR15663505_1.fastq.gz	Fastqsanger.gz

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Transcription factors Bcl11a and Bcl11b are Required for the production and differentiation of cortical projection neurons

Project description:Purpose:To assess changes in gene expression profiles of single cell from the wild type littermate controls cortices in E13.5, E15.5 and P0, and conditional knockout Bcl11a (and Bcl11b) at cortical projection neurons in the mouse cortices of the same ages. Methods: E13.5, E15.5 and P0 control and mutant cortices were carefully dissected under a clean environment. Then total RNA was isolated using an RNeasy Mini Kit (QIAGEN) according to the manufacturer’s protocol, quantified using NanoDrop ND-2000, and checked for RNA integrity using Agilent 2100 bioanalyzer. RNA-seq libraries were prepared according to the Illumina TruSeq protocol. Results: An average of 15 million reads per sample were obtained.

2021-08-31 | GSE182990 | GEO

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway II

Project description:Developmental neuron death plays a pivotal role in refining organization and wiring during neocortex formation. Aberrant regulation of this process results in neurodevelopmental disorders including impaired learning and memory. Underlying molecular pathways are incompletely determined. Loss of Bcl11a in cortical projection neurons induces pronounced cell death in upper-layer cortical projection neurons during postnatal corticogenesis. We used this genetic model to explore genetic mechanisms by which developmental neuron death is controlled. Unexpectedly, we found Bcl6, previously shown to be involved in transition of cortical neurons from progenitor to postmitotic differentiation state to provide a major check point regulating neuron survival during late cortical development. We show that Bcl11a is a direct transcriptional regulator of Bcl6. Deletion of Bcl6 exerts death of cortical projection neurons. In turn, reintroduction of Bcl6 into Bcl11a mutants prevents induction of cell death in these neurons. Together, our data identify a novel Bcl11a/Bcl6-dependent molecular pathway in regulation of developmental cell death during corticogenesis.

2022-06-24 | GSE185288 | GEO

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway I

2022-06-24 | GSE185287 | GEO

Transcription factors Bcl11a and Bcl11b are required for the production and differentiation of cortical projection neurons.

Project description:The generation and differentiation of cortical projection neurons are extensively regulated by interactive programs of transcriptional factors. Here, we report the cooperative functions of transcription factors Bcl11a and Bcl11b in regulating the development of cortical projection neurons. Among the cells derived from the cortical neural stem cells, Bcl11a is expressed in the progenitors and the projection neurons, while Bcl11b expression is restricted to the projection neurons. Using conditional knockout mice, we show that deficiency of Bcl11a leads to reduced proliferation and precocious differentiation of cortical progenitor cells, which is exacerbated when Bcl11b is simultaneously deleted. Besides defective neuronal production, the differentiation of cortical projection neurons is blocked in the absence of both Bcl11a and Bcl11b: Expression of both pan-cortical and subtype-specific genes is reduced or absent; axonal projections to the thalamus, hindbrain, spinal cord, and contralateral cortical hemisphere are reduced or absent. Furthermore, neurogenesis-to-gliogenesis switch is accelerated in the Bcl11a-CKO and Bcl11a/b-DCKO mice. Bcl11a likely regulates neurogenesis through repressing the Nr2f1 expression. These results demonstrate that Bcl11a and Bcl11b jointly play critical roles in the generation and differentiation of cortical projection neurons and in controlling the timing of neurogenesis-to-gliogenesis switch.

| S-EPMC9433425 | biostudies-literature

Bcl11a (Ctip1) controls migration of cortical projection neurons through regulation of Sema3c

Project description:During neocortical development, neurons undergo polarization, oriented migration, and layer type-specific differentiation. The transcriptional programs underlying these processes are not completely understood. Here we show that the transcription factor Bcl11a regulates polarity and migration of upper layer neurons. Bcl11a-deficient late-born neurons fail to correctly switch from multipolar to bipolar morphology resulting in impaired radial migration. We show that the expression of Sema3c is increased in migrating Bcl11a-deficient neurons and that Bcl11a is a direct negative regulator of Sema3c transcription. In vivo gain-of-function and rescue experiments demonstrate that Sema3c is a major downstream effector of Bcl11a required for the cell polarity switch and for the migration of upper layer neurons. Our data uncover a novel Bcl11a/Sema3c-dependent regulatory pathway used by migrating cortical neurons. Neocortex tissue from three control (Bcl11a+/+) and three Bcl11a mutants (Bcl11aΔflox/Δflox) embryos was collected at E14.5. Total RNA was isolated from each sample separately using the RNeasy kit (Qiagen). The isolated ENA was inspected for integrity and purity using an Agilent Bioanalyzer and a NanoDrop spectrophotometer, respectively. Microarray analyses were performed using 200 ng total RNA as starting material and 5.5 µg ssDNA per hybridization in a GeneChip Fluidics Station 450 (Affymetrix). The total RNAs were amplified and labeled following the Whole Transcript (WT) Sense Target Labeling Assay (Affymetrix). Labeled ssDNA was hybridized to Mouse Gene 1.0 ST Affymetrix GeneChip arrays (Affymetrix). The chips were scanned with a GeneChip Scanner 3000 (Affymetrix) and subsequent images analyzed using Affymetrix Expression Console Software (Affymetrix). A transcriptome analysis was performed using BRB-ArrayTools developed by Dr. Richard Simon and BRB-ArrayTools Development Team (http://linus.nci.nih.gov/BRB-ArrayTools.html).

2015-06-17 | E-GEOD-52827 | biostudies-arrayexpress

Bcl11a (Ctip1) controls migration of cortical projection neurons through regulation of Sema3c

2015-06-17 | GSE52827 | GEO

Transcription profiling of mouse FACS-purified cortical projection neurons

Project description:This SuperSeries is composed of the following subset Series:; GSE2039: FACS purified cortical projection neurons; GSE17783: Analysis of gene expression in FACS-purified cortical projection neurons using Affymetrix 430 2.0 microarrays Experiment Overall Design: Refer to individual Series

2009-10-10 | E-GEOD-17784 | biostudies-arrayexpress

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway II

Project description:Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway II

| PRJNA768460 | ENA

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway I

Project description:Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway I

| PRJNA768459 | ENA

Transcription profiling of mouse FACS purified cortical projection neurons

Project description:3 subtypes of cortical projection neurons were purified by fluorescence-activated cell sorting at 4 different stages of development from mouse cortex. A detailed description of the data set is described in Arlotta, P et al (2005)

2007-11-20 | E-GEOD-2039 | biostudies-arrayexpress

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