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Foxp1 suppresses cortical angiogenesis and attenuates HIF-1alpha signaling to promote neural progenitor cell maintenance.

ABSTRACT: To investigate the function of Foxp1 in the regulation of radial glial differentiation, we established Foxp1flox/flox;Emx1Cre mouse line in which Foxp1 is removed in cortical radial glia. We then performed gene expression profiling analysis using data obtained from bulk RNA-seq of 4 Cre negative controls and 2 mutants at E12.5.

ORGANISM(S): Mus musculus

PROVIDER: GSE217364 | GEO | 2024/04/22

REPOSITORIES: GEO

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Foxp1 suppresses cortical angiogenesis and attenuates HIF-1alpha signaling to promote neural progenitor cell maintenance.

Project description:Neural progenitor cells within the cerebral cortex undergo a characteristic switch between symmetric self-renewing cell divisions early in development and asymmetric neurogenic divisions later. Yet, the mechanisms controlling this transition remain unclear. Previous work has shown that early but not late neural progenitor cells (NPCs) endogenously express the autism-linked transcription factor Foxp1, and both loss and gain of Foxp1 function can alter NPC activity and fate choices. Here, we show that premature loss of Foxp1 upregulates transcriptional programs regulating angiogenesis, glycolysis, and cellular responses to hypoxia. These changes coincide with a premature destabilization of HIF-1α, an elevation in HIF-1α target genes, including Vegfa in NPCs, and precocious vascular network development. In vitro experiments demonstrate that stabilization of HIF-1α in Foxp1-deficient NPCs rescues the premature differentiation phenotype and restores NPC maintenance. Our data indicate that the endogenous decline in Foxp1 expression activates the HIF-1α transcriptional program leading to changes in the tissue environment adjacent to NPCs, which, in turn, might alter their self-renewal and neurogenic capacities.

| S-SCDT-10_1038-S44319-024-00131-8 | biostudies-other

Foxp1 suppresses cortical angiogenesis and attenuates HIF-1alpha signaling to promote neural progenitor cell maintenance.

Project description:Foxp1 suppresses cortical angiogenesis and attenuates HIF-1alpha signaling to promote neural progenitor cell maintenance.

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FOXP1-SHQ1 deletion cooperates with PTEN deletion in oncogenesis

Project description:RNA-seq was carried out on prostate tumors from mice with prostate-conditional PTEN knockout with and without prostate-conditional FOXP1-SHQ1 locus deletion (12 month old PTEN-flox/flox Pb-Cre4 mice and FOXP1-SHQ1-flox/flox PTEN-flox/flox Pb-Cre4 mice )

2017-09-08 | GSE83358 | GEO

FOXP1 inhibits cell growth and attenuates tumorigenicity of neuroblastoma

Project description:Single-color gene expression profiles from 3 neuroblastoma cell lines were generated using 44K oligonucleotide microarrays. To gain insights into the molecular processes occurring upon FOXP1 re-expression, we performed series of time-resolved gene expression measurements in FOXP1 and GFP transgenic neuroblastoma cell lines. Single-color gene expression profiles from 3 neuroblastoma cell lines were generated using 44K oligonucleotide microarrays. Total RNA of FOXP1- and GFP-expressing IMR-32, CHP-212 and SK-N-BE(2) cells was isolated at 0, 12, 24 and 72 h using Trizol. To determine global differences in the expression profiles of FOXP1- and GFP-induced IMR-32, CHP-212 and SK-N-BE(2) cells, mean expression levels of each gene between FOXP1-induced and control (GFP) cells were compared.

2014-10-17 | E-GEOD-62419 | biostudies-arrayexpress

FOXP1 inhibits cell growth and attenuates tumorigenicity of neuroblastoma

2014-10-17 | GSE62419 | GEO

Transcriptome profiling of WT and Prdm16 mutant cells in embryonic mouse cerebral cortex.

Project description:Transcriptome profiling of radial glia, intermediate progenitors, and cortical neurons in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.

2018-06-21 | GSE111660 | GEO

Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [Foxp1 cTG scRNA-seq]

Project description:Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.

2023-02-15 | GSE222956 | GEO

Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [Foxp1 cKO bulk RNA-seq]

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Non-IG Aberrations of FOXP1 in B-Cell Malignancies Lead to an Aberrant Expression of N-Truncated Isoforms of FOXP1

Project description:The transcription factor FOXP1 is implicated in the pathogenesis of B-cell lymphomas through immunoglobulin heavy chain (IGH) locus-related chromosomal translocations leading to dysregulated expression of FOXP1. Translocations of FOXP1 with non-IG gene sequences have been also reported, but the molecular consequences of such aberrations remain undetermined. Here, using molecular cytogenetics and molecular biology studies, we comprehensively analyzed four lymphoma cases with non-IG rearrangements of FOXP1 and compared these with cases harboring t(3;14)(p13;q32)/IGH-FOXP1 and FOXP1-expressing lymphomas without underlying t(3p13/FOXP1). We found that non-IG rearrangements are usually acquired during evolution of lymphoma and constantly target the coding region of FOXP1, promiscuously fusing with coding and non-coding gene sequences at various reciprocal breakpoints (2q36, 10q24 and 3q11). Intriguingly, these rearrangements do not generate functional chimeric genes but commonly disrupt the full-length FOXP1 transcript leading to an aberrant expression of N-truncated FOXP1 isoforms, as shown by QRT-PCR and Western blot analysis. In contrast, cases with t(3;14)(p13;q32)/IGH-FOXP1 overexpress the full-length FOXP1. Collectively, our findings point to a dual mechanism through which FOXP1 is implicated in B-cell lymphomagenesis. The primary t(3;14)(p13;q32)/IGH-FOXP1 produces the full-length protein with potent oncogenic activity, whereas the secondary non-IG 17 rearrangements of FOXP1 generate N-truncated FOXP1 isoforms, likely driving progression of disease. Using molecular cytogenetics and molecular biology studies (including RNA-seq), we comprehensively analyzed four lymphoma cases with non-IG rearrangements of FOXP1 and compared these with cases harboring t(3;14)(p13;q32)/IGH-FOXP1 and FOXP1-expressing lymphomas without underlying t(3p13/FOXP1).

2013-09-04 | E-GEOD-50514 | biostudies-arrayexpress