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Downstream targeted genes of Satb2 regulate synaptic formation and axonogenesis in developing cerebral cortex

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE201562 | GEO | 2022/08/24

REPOSITORIES: GEO

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

2022-08-23 | GSE201433 | GEO

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

2022-08-25 | GSE201561 | GEO

Downstream targeted genes of Satb2 regulate synaptic formation and axonogenesis in developing cerebral cortex

Project description:Downstream targeted genes of Satb2 regulate synaptic formation and axonogenesis in developing cerebral cortex

| PRJNA832224 | ENA

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

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

| PRJNA831785 | ENA

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

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

| PRJNA832225 | ENA

Mutual regulation between Satb2 and Fezf2 promotes subcerebral projection neuron identity in the developing cerebral cortex.

Project description:Generation of distinct cortical projection neuron subtypes during development relies in part on repression of alternative neuron identities. It was reported that the special AT-rich sequence-binding protein 2 (Satb2) is required for proper development of callosal neuron identity and represses expression of genes that are essential for subcerebral axon development. Surprisingly, Satb2 has recently been shown to be necessary for subcerebral axon development. Here, we unravel a previously unidentified mechanism underlying this paradox. We show that SATB2 directly activates transcription of forebrain embryonic zinc finger 2 (Fezf2) and SRY-box 5 (Sox5), genes essential for subcerebral neuron development. We find that the mutual regulation between Satb2 and Fezf2 enables Satb2 to promote subcerebral neuron identity in layer 5 neurons, and to repress subcerebral characters in callosal neurons. Thus, Satb2 promotes the development of callosal and subcerebral neurons in a cell context-dependent manner.

| S-EPMC4577201 | biostudies-literature

Satb2 Regulates the Differentiation of Both Callosal and Subcerebral Projection Neurons in the Developing Cerebral Cortex.

Project description:The chromatin-remodeling protein Satb2 plays a role in the generation of distinct subtypes of neocortical pyramidal neurons. Previous studies have shown that Satb2 is required for normal development of callosal projection neurons (CPNs), which fail to extend axons callosally in the absence of Satb2 and instead project subcortically. Here we conditionally delete Satb2 from the developing neocortex and find that neurons in the upper layers adopt some electrophysiological properties characteristic of deep layer neurons, but projections from the superficial layers do not contribute to the aberrant subcortical projections seen in Satb2 mutants. Instead, axons from deep layer CPNs descend subcortically in the absence of Satb2. These data demonstrate distinct developmental roles of Satb2 in regulating the fates of upper and deep layer neurons. Unexpectedly, Satb2 mutant brains also display changes in gene expression by subcerebral projection neurons (SCPNs), accompanied by a failure of corticospinal tract (CST) formation. Altering the timing of Satb2 ablation reveals that SCPNs require an early expression of Satb2 for differentiation and extension of the CST, suggesting that early transient expression of Satb2 in these cells plays an essential role in development. Collectively these data show that Satb2 is required by both CPNs and SCPNs for proper differentiation and axon pathfinding.

| S-EPMC4585495 | biostudies-literature

Protocadherin 8 and transcription factor Dbx1 regulate the formation of developing cerebral cortex

Project description:Normal development of the mammalian central nervous system requires correct tissue patterning, production of the appropriate cell types and establishment of functional neuronal circuits. Transcription factors (TFs) play essential roles in these processes, regulating the expression of target genes responsible for neuronal subtypes specific features. Cell adhesion molecules are key components of neuronal identities that control cell sorting, migration, neurite outgrowth/guidance and synaptogenesis. So far, the link between cell adhesion and cell fate is not known TFs are known to control neuronal adhesion but not the opposite. Here, using acute gain- and loss-of-function experiments by in utero electroporation in the developing mouse telencephalon we demonstrate that ectopic expression of Dbx1, a homeodomain TF acting as a cell fate determinant, leads to increased expression of Protocadherin 8 (Pcdh8) and cell aggregation, together with the induction of neuronal fate markers Nr4a2 (Nurr1) and Pax6. These effects were are modulated depending on the region and timing of electroporation. Furthermore, we found that Pcdh8 expression is required for Dbx1-induced fate specification. Surprisingly, Pcdh8 overexpression also proved sufficient to induce Dbx1 expression as well as a complete reorganisation of the apico-basal polarity and dorso-ventral patterning. Finally, we present evidence that these effects are mediated through regulation of the expression of Notch ligands and promotion of cell cycle exit. Altogether, our work therefore points to cell adhesion molecules as unexpectedimportant, yet unexpected important, players in the regulation of cell identity and, in particular, Pcdh8 through its bidirectional action crossregulation with the Dbx1 transcription factor.

2024-10-13 | GSE229603 | GEO

Mutual Regulation between Satb2 and Fezf2 Promotes Subcerebral Projection Neuron Identity in the Developing Cerebral Cortex

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-08 | E-GEOD-68912 | biostudies-arrayexpress

Glutathione S-transferase Pi (Gstp) proteins regulate neuritogenesis in the developing cerebral cortex.

Project description:GSTP proteins are metabolic enzymes involved in the removal of oxidative stress and intracellular signaling and also have inhibitory effects on JNK activity. However, the functions of Gstp proteins in the developing brain are unknown. In mice, there are three Gstp proteins, Gstp1, 2 and 3, whereas there is only one GSTP in humans. By reverse transcription-polymerase chain reaction (RT-PCR) analysis, we found that Gstp1 was expressed beginning at E15.5 in the cortex, but Gstp2 and 3 started expressing at E18.5. Gstp 1 and 2 knockdown (KD) caused decreased neurite number in cortical neurons, implicating them in neurite initiation. Using in utero electroporation (IUE) to knock down Gstp1 and 2 in layer 2/3 pyramidal neurons in vivo, we found abnormal swelling of the apical dendrite at P3 and reduced neurite number at P15. Using time-lapse live imaging, we found that the apical dendrite orientation was skewed compared with the control. We explored the molecular mechanism and found that JNK inhibition rescued reduced neurite number caused by Gstp knockdown, indicating that Gstp regulates neurite formation through JNK signaling. Thus, we found novel functions of Gstp proteins in neurite initiation during cortical development. These findings not only provide novel functions of Gstp proteins in neuritogenesis during cortical development but also help us to understand the complexity of neurite formation.

| S-EPMC8033146 | biostudies-literature

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