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Downstream targeted genes of Satb2 regulate synaptic formation and axonogenesis in developing cerebral cortex [ChIP-seq]

ABSTRACT: Special AT-rich sequencebinding protein 2 (SATB2) is essential for the development of cerebral cortex and key molecular node for the establishment of proper neural circuitry and function. Mutations in SATB2 gene lead to SATB2-associated syndrome (SAS), which is characterized by abnormal development of skeleton and central nervus system. We generated Satb2 knockout mouse model through CRISPR-Cas9 technology and performed RNA-seq and ChIP-seq of embryonic cerebral cortex. We conducted RT-qPCR, western blot, immunofluorescence staining, luciferase reporter assay and behavioral analysis for experimental verification.

ORGANISM(S): Mus musculus

PROVIDER: GSE201433 | GEO | 2022/08/23

REPOSITORIES: GEO

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Downstream targeted genes of Satb2 regulate synaptic formation and axonogenesis in developing cerebral cortex [RNA-seq]

Project description:Special AT-rich sequencebinding protein 2 (SATB2) is essential for the development of cerebral cortex and key molecular node for the establishment of proper neural circuitry and function. Mutations in SATB2 gene lead to SATB2-associated syndrome (SAS), which is characterized by abnormal development of skeleton and central nervus system. We generated Satb2 knockout mouse model through CRISPR-Cas9 technology and performed RNA-seq and ChIP-seq of embryonic cerebral cortex. We conducted RT-qPCR, western blot, immunofluorescence staining, luciferase reporter assay and behavioral analysis for experimental verification.

2022-08-25 | GSE201561 | GEO

ChIP-seq for Satb2 in E15 cortex

Project description:The goal of the study was to identify the binding site of SATB2 in wild-ype cortex by performing ChIP-seq using SATB2 antibody. E15 cortical tissues were dissected, lysed and fixed. Chromatin was prepared by sonication. Sequences bound by SATB2 protein was precipitated using a SATB2 antibody. Sequencing was performed on Illumina Genome Analyzer II. SATB2 binding peaks were called using MACS. ChIP for Satb2, followed by sequencing on Illumina Genome Analyzer II platform

2015-09-08 | E-GEOD-68910 | biostudies-arrayexpress

ChIP-seq for Satb2 in E15 cortex

2015-09-08 | GSE68910 | GEO

Investigation into SATB2 DNA-binding sites and the effect of SATB2 removal on the transcriptome of skeletal muscle satellite cells

Project description:Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. In our associated paper, we found that the removal of special AT-rich binding protein 2 (SATB2), a nuclear protein that binds matrix attachment regions, is a key event in initiating myogenic differentiation. This study included ChIP-seq analyses to assess the genetic binding sites of SATB2 prior to differentiation and categorize their respective roles within the cell. Furthermore, transcriptome analyses using RNA-seq was conducted on C2C12 cells treated with control siRNA and siRNA against SATB2 prior to differentiation. This was done to assess the changes in transcript expression following the loss of SATB2.

2023-04-06 | GSE148193 | GEO

SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells

Project description:The special AT-rich sequence-binding protein 2 (SATB2) is a protein that binds to the nuclear matrix attachment region of the cell and regulates gene expression by altering chromatin structure. We show that ectopic expression of SATB2 in normal human bronchial epithelial cell-line BEAS2B increased anchorage-independent growth and cell migration,RNA sequencing analyses of SATB2 regulated genes revealed the enrichment of those involved in cytoskeleton, cell adhesion and cell-movement pathways.

2016-02-01 | GSE75652 | GEO

Chromatin reorganization during myoblast differentiation involves the caspase-dependent removal of SATB2 [RNA-seq]

Project description:Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. Here, we report that removal of special AT-rich binding protein 2 (SATB2), a nuclear protein known to bind matrix attachment regions, is a key event in initiating myogenic differentiation. Deletion of myoblast SATB2 in vitro initiates chromatin remodeling and accelerates differentiation, while in vivo ablation depletes the muscle progenitor pool. Genome wide analysis indicates that SATB2 binding influences both chromatin loop and sub-TAD domain formation. These chromatin changes are both repressive and inductive, as loss of SATB2 leads to expression of differentiation regulatory factors and inhibition of genes that impair this process. Finally, we noted that the differentiation-specific decline in SATB2 protein is dependent on a caspase 7-mediated cleavage event. Taken together, this study demonstrates that temporal control of SATB2 protein is critical for shaping the chromatin environment and coordinating the myogenic differentiation program

2022-03-31 | GSE185436 | GEO

Chromatin reorganization during myoblast differentiation involves the caspase-dependent removal of SATB2 [ChIP-seq]

Project description:Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. Here, we report that removal of special AT-rich binding protein 2 (SATB2), a nuclear protein known to bind matrix attachment regions, is a key event in initiating myogenic differentiation. Deletion of myoblast SATB2 in vitro initiates chromatin remodeling and accelerates differentiation, while in vivo ablation depletes the muscle progenitor pool. Genome wide analysis indicates that SATB2 binding influences both chromatin loop and sub-TAD domain formation. These chromatin changes are both repressive and inductive, as loss of SATB2 leads to expression of differentiation regulatory factors and inhibition of genes that impair this process. Finally, we noted that the differentiation-specific decline in SATB2 protein is dependent on a caspase 7-mediated cleavage event. Taken together, this study demonstrates that temporal control of SATB2 protein is critical for shaping the chromatin environment and coordinating the myogenic differentiation program

2022-03-31 | GSE185435 | GEO

Chromatin reorganization during myoblast differentiation involves the caspase-dependent removal of SATB2 [Hi-C]

Project description:Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. Here, we report that removal of special AT-rich binding protein 2 (SATB2), a nuclear protein known to bind matrix attachment regions, is a key event in initiating myogenic differentiation. Deletion of myoblast SATB2 in vitro initiates chromatin remodeling and accelerates differentiation, while in vivo ablation depletes the muscle progenitor pool. Genome wide analysis indicates that SATB2 binding influences both chromatin loop and sub-TAD domain formation. These chromatin changes are both repressive and inductive, as loss of SATB2 leads to expression of differentiation regulatory factors and inhibition of genes that impair this process. Finally, we noted that the differentiation-specific decline in SATB2 protein is dependent on a caspase 7-mediated cleavage event. Taken together, this study demonstrates that temporal control of SATB2 protein is critical for shaping the chromatin environment and coordinating the myogenic differentiation program

2022-03-31 | GSE185434 | GEO

Gene expression signatures of SATB2-defficient vs wild-type adult neocortex

Project description:During CNS development, the nuclear protein SATB2 is expressed in superficial cortical layers and determines projection neuron identity. In the adult CNS, SATB2 is expressed in pyramidal neurons of all cortical layers and is a regulator of synaptic plasticity and long-term memory. Common variation in SATB2 locus confers risk of schizophrenia whereas rare, de novo structural and single nucleotide variants cause severe intellectual disability and absent or limited speech. To which extent symptoms in SATB2-related human pathologies depend on developmental or adult functions of the protein remains to be established. To characterize differences in SATB2 molecular function in developing vs adult neocortex, we compared SATB2 protein interactomes and SATB2-driven gene expression programs at the two ontogenetic stages by co-IP mass spectrometry and RNAseq analyses, respectively. Our results demonstrated that 1) SATB2 interacts with different protein networks at the two ontogenetic stages, with a switch from transcriptional repression towards organization of chromatin structure and 2) SATB2 determines differential transcriptional programs in neonatal vs adult cortex.

2019-02-19 | GSE123992 | GEO

Role of Satb1 and Satb2 in embryonic stem cells

Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. This SuperSeries is composed of the following subset Series: GSE17487: Expression data in WT and Satb1-/- ES cells GSE17488: Expression data in WT and ES cells overexpressing Satb1 GSE17489: Expression data in WT and ES cells overexpressing Satb2 Refer to individual Series

2009-09-01 | E-GEOD-17490 | biostudies-arrayexpress

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