ArticleCell death and differentiation2020
Satb2 is required for the regionalization of retrosplenial cortex.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Essential function of Nr4a2 in subicular development and social novelty.Journal of advanced research · 2026Article
- Hippocampal Satb2 regulates the cognitive function of adult mice through pleiotrophin.Cell death & disease · 2026Article
- Uncovering causal relationships in single-cell omic studies with causarray.Briefings in bioinformatics · 2026Article
- Pbx1 and Pbx3 cooperatively regulate intermediate progenitor genesis and corticogenesis in the mouse neocortex.Frontiers in cell and developmental biology · 2026Article
- Advances in research on SATB2 and its role in tumor development.Cell & bioscience · 2025Review
- Satb2 and Nr4a2 are required for the differentiation of cortical layer 6b.Cell death discovery · 2025Article
- Development of Differential Sublaminar Feedforward Inhibitory Circuits in CA1 Hippocampus RequiresThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Spatial transcriptome reveals the region-specific genes and pathways regulated by Satb2 in neocortical development.BMC genomics · 2024Article
- The spatiotemporal dynamics of spatially variable genes in developing mouse brain revealed by a novel computational scheme.Cell death discovery · 2023Article
- Overexpression of EphB6 and EphrinB2 controls soma spacing of cortical neurons in a mutual inhibitory way.Cell death & disease · 2023Article
- FOXG1 drives transcriptomic networks to specify principal neuron subtypes during the development of the medial pallium.Science advances · 2023Article
- RNF220 is an E3 ubiquitin ligase for AMPA receptors to regulate synaptic transmission.Science advances · 2022Article
- Deletion of Schizophrenia Susceptibility Gene Ulk4 Leads to Abnormal Cognitive Behaviors via Akt-GSK-3 Signaling Pathway in Mice.Schizophrenia bulletin · 2022Article
- Satb2 acts as a gatekeeper for major developmental transitions during early vertebrate embryogenesis.Nature communications · 2021Article
- Satb2 regulates the development of dopaminergic neurons in the arcuate nucleus by Dlx1.Cell death & disease · 2021Article
- Article
- Programmed suppression of oxidative phosphorylation and mitochondrial function by gestational alcohol exposure correlate with widespread increases in H3K9me2 that do not suppress transcription.Epigenetics & chromatin · 2021Article
- Developmental Patterning and Neurogenetic Gradients ofFrontiers in neuroanatomy · 2021Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retrosplenial cortex (Rsp) is a transitional cortex located between the neocortex and archicortex, but the molecular mechanism specifying Rsp from the archicortex remains elusive. We here report that the transcription factor Satb2 is required for specifying Rsp identity during its morphogenesis. In Satb2 CKO mice, the boundary between the Rsp and archicortex [i.e., subiculum (SubC)] disappears as early as E17.5, and Rsp efferent projection is aberrant. Rsp-specific genes are lost, whereas SubC-specific genes are ectopically expressed in Rsp of Satb2 CKO mice. Furthermore, cell-autonomous role of Satb2 in maintaining Rsp neuron identity is revealed by inactivation of Satb2 in Rsp neurons. Finally, Satb2 represses the transcription of Nr4a2. The misexpression of Nr4a2 together with Ctip2 induces expression of SubC-specific genes in wild-type Rsp, and simultaneous knockdown of these two genes in Rsp Satb2-mutant cells prevents their fate transition to SubC identity. Thus, Satb2 serves as a determinant gene in the Rsp regionalization by repressing Nr4a2 and Ctip2 during cortical development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.