Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]
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PROVIDER: PRJNA549718 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptome analysis following Bcl6 induction (24h doxycycline) in mouse ES-cell-derived cortical progenitors (differentiation day 12) shows that Bcl6 promotes a neurogenic transcription program and represses selective genes of the main proliferative pathways.
2019-06-20 | GSE133031 | GEO
Project description:Bcl6 binding sites and neurogenic activity in in vitro cortical progenitors
| PRJNA549714 | ENA
Project description:Chromatin immunoprecipitation following Bcl6 induction (24h doxycycline) in mouse ES-cell-derived cortical progenitors (differentiation day 12).
2019-06-20 | GSE132964 | GEO
Project description:Bcl6 binding sites in in vitro cortical progenitors [ChIP-Seq]
| PRJNA549710 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-06-20 | GSE133032 | GEO
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
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 | GSE185287 | GEO
Project description:The molecular basis for cortical expansion during evolution remains largely unknown. Here, we report that fibroblast growth factor (FGF)-extracellular signal-regulated kinase (ERK) signaling promotes the self-renewal and expansion of cortical radial glial (RG) cells. Furthermore, FGF-ERK signaling induces bone morphogenic protein 7 (Bmp7) expression in cortical RG cells, which increases the length of the neurogenic period. We demonstrate that ERK signaling and Sonic Hedgehog (SHH) signaling mutually inhibit each other in cortical RG cells. We provide evidence that ERK signaling is elevated in cortical RG cells during development and evolution. We propose that the expansion of the mammalian cortex, notably in human, is driven by the ERK-BMP7-GLI3R signaling pathway in cortical RG cells, which participates in a positive feedback loop through antagonizing SHH signaling. We also propose that the relatively short cortical neurogenic period in mice is partly due to mouse cortical RG cells receiving higher SHH signaling that antagonizes ERK signaling.
2023-08-09 | GSE240381 | GEO
Project description:With advancing age, senescent cells accumulate as they are not efficiently cleared by the immune system anymore. Via a senescence-associated secretory phenotype, chronic senescent cells alter the microenvironment, creating an unfavorable milieu for neurogenesis and neurorepair. Using an innovative and rapid aging model, the African turquoise killifish, we have previously demonstrated a dramatic decline in neurogenic potential of non-glial progenitors with age. Even after traumatic brain injury, progenitor proliferation and neuron production was very low in aged killifish in comparison to young adult killifish, and overall neurorepair was incomplete. In the present study, we validated if the senolytic cocktail dasatinib and quercetin (D+Q) could reboot the neurogenic output by clearing chronic senescent cells from the aged killifish brain to re-create the necessary supportive environment. Our results confirm that the aged killifish telencephalon holds a very high senescent cell burden, which we could diminish by short-term systemic D+Q treatment. As a consequence of D+Q administration, proliferation of non-glial progenitors increased and more new neurons were generated and migrated into the parenchyma after injury. Injury-induced inflammation and glial scarring, a phenomenon only seen in aged killifish, remained unaltered. Senolytic treatment with D+Q might thus hold promise for improving brain function in aged populations, and is especially interesting for reviving the neurogenic potential of an already aged central nervous system.
2023-07-20 | PXD036437 | Pride
Project description:Asymmetric neuronal expansion is thought to drive evolutionary transitions from lissencephalic to gyrencephalic cerebral cortices. We report that Neurog2 and Ascl1 proneural genes interact to sustain neurogenic continuity and lissencephaly in rodents. Using transgenic reporter mice and human cerebral organoids, we found that Neurog2 and Ascl1 expression defines a continuum of four lineage-biased neural progenitor cell (NPC) pools. Double+ NPCs, at the hierarchical apex, are least lineage-restricted due to Neurog2-Ascl1 cross-repression, and display unique features of multipotency (more open chromatin, complex gene regulatory network, G2 pausing). Strikingly, selective killing of double+ NPCs using Neurog2-Ascl1 split-Cre mice and three ‘deletor’ strains breaks neurogenic symmetry by locally disrupting Notch signaling, leading to cortical folding. Consistent with proneural genes driving discontinuous neurogenesis and folding via Notch, NEUROG2, ASCL1 and HES1 transcripts are modular in gyrencephalic macaque cortices. Neurog2/Ascl1 double+ NPCs are thus Notch-ligand expressing ‘niche’ cells that control neurogenic periodicity and cortical gyrification.
2021-07-08 | GSE151775 | GEO