Similar Datasets
Project description:The HMG-domain containing SoxC transcription factors Sox4 and Sox11 are expressed in the vertebrate central nervous system in neuronal precursors and neuroblasts. They are required during early stages of neurogenesis. Here we perform micorarray analysis to identify genes that are downstream of these SoxC proteins during spinal cord neurogenesis in mouse. The identified genes represent potential direct target genes of Sox4 and Sox11.
2018-05-10 | GSE106786 | GEO
Project description:The HMG-domain containing SoxC transcription factors Sox4 and Sox11 are expressed in the vertebrate central nervous system in neuronal precursors and neuroblasts. They are required during early stages of neurogenesis. Here we perform micorarray analysis to identify genes that are downstream of these SoxC proteins during spinal cord neurogenesis in chicken. The identified genes represent potential direct target genes of Sox4 and Sox11.
2018-05-10 | GSE106787 | GEO
Project description:Identification of SoxC-regulated genes during neurogenesis in the developing spinal cord
| PRJNA418039 | ENA
Project description:Identification of SoxC-regulated genes during neurogenesis in the developing spinal cord [chicken]
| PRJNA418041 | ENA
Project description:Identification of SoxC-regulated genes during neurogenesis in the developing spinal cord [mouse]
| PRJNA418040 | ENA
Project description:Various types of neurons and glia are generated following a precise spatial and temporal order during neurogenesis. The mechanisms that control this sequential generation of neuronal and glial cell types from the same progenitor population are not well understood. Growth differentiation factor 11 (Gdf11) belongs to the TGF-? family of proteins and is expressed transiently in newly born neurons adjacent to the progenitor domain in the developing spinal cord. We examined the phenotypes of Gdf11(-/-) mouse embryos and found that without Gdf11, neuronal differentiation in the spinal cord progresses at a slower rate. Higher progenitor proliferation rate, along with a delay in gliogenesis, is also observed in Gdf11(-/-) spinal cord but only after the peak of Gdf11 expression, indicating that Gdf11 can cause long-lasting changes in progenitor properties. These changes can be preserved in vitro, as neurospheres derived from Gdf11(-/-) and wild-type littermates at a stage after, but not before the onset of Gdf11 expression, exhibit differences in proliferation and differentiation potential. Moreover, these changes in progenitor properties can be induced in vitro by the addition of Gdf11. We also demonstrate that the effects of Gdf11 on progenitor cells are associated with its ability to upregulate p57(Kip2) and p27(Kip1) while downregulating Pax6 expression. These results support a model in which Gdf11 secreted by newly born neurons in the developing spinal cord facilitates the temporal progression of neurogenesis by acting as a positive feedback signal on the progenitor cells to promote cell cycle exit and decrease proliferation ability, thus changing their differentiation potential.
| S-EPMC4112097 | biostudies-literature
Project description:Wnt/FZD signalling activity is required for spinal cord development, including the dorsal-ventral patterning of the neural tube, where it affects proliferation and specification of neurons. Wnt ligands initiate canonical, β -catenin-dependent, signaling by binding to Frizzled receptors. However, in many developmental contexts the cognate FZD receptor for a particular Wnt ligand remains to be identified. Here, we characterized FZD10 expression in the dorsal neural tube where it overlaps with both Wnt1 and Wnt3a, as well as markers of dorsal progenitors and interneurons. We show FZD10 expression is sensitive to Wnt1, but not Wnt3a expression, and FZD10 plays a role in neural tube patterning. Knockdown approaches show that Wnt1 induced ventral expansion of dorsal neural markes, Pax6 and Pax7, requires FZD10. In contrast, Wnt3a induced dorsalization of the neural tube is not affected by FZD10 knockdown. Gain of function experiments show that FZD10 is not sufficient on its own to mediate Wnt1 activity in vivo. Indeed excess FZD10 inhibits the dorsalizing activity of Wnt1. However, addition of the Lrp6 co-receptor dramatically enhances the Wnt1/FZD10 mediated activation of dorsal markers. This suggests that the mechanism by which Wnt1 regulates proliferation and patterning in the neural tube requires both FZD10 and Lrp6.
| S-EPMC7292682 | biostudies-literature
Project description:Neural stem and progenitor cells undergo an important transition from proliferation to differentiation in the G1 phase of the cell cycle. The mechanisms coordinating this transition are incompletely understood. Cyclin D proteins promote proliferation in G1 and typically are down-regulated before differentiation. Here we show that motoneuron progenitors in the embryonic spinal cord persistently express Cyclin D1 during the initial phase of differentiation, while down-regulating Cyclin D2. Loss-of-function and gain-of-function experiments indicate that Cyclin D1 (but not D2) promotes neurogenesis in vivo, a role that can be dissociated from its cell cycle function. Moreover, reexpression of Cyclin D1 can restore neurogenic capacity to D2-expressing glial-restricted progenitors. The neurogenic function of Cyclin D1 appears to be mediated, directly or indirectly, by Hes6, a proneurogenic basic helic-loop-helix transcription factor. These data identify a cell cycle-independent function for Cyclin D1 in promoting neuronal differentiation, along with a potential genetic pathway through which this function is exerted.
| S-EPMC3136279 | biostudies-literature
Project description:In the developing CNS, neurons and glia are sequentially produced from the ventricular neural progenitor cells. One fundamental question in developmental neurobiology is what signals or factors control the developmental switch from neurogenesis to gliogenesis. Here we report that microRNAs (miRNAs) play an essential role in this important developmental process. Inhibition of miRNA formation in Olig1(Cre)-mediated Dicer conditional knock-out mice disrupted both oligodendrogenesis and astrogliogenesis in the ventral neuroepithelial cells. By contrast, the early patterning and development of motor neurons were not affected in the mutant spinal cord tissue.
| S-EPMC2918643 | biostudies-literature
Project description:Neurogenesis requires the coordination of neural progenitor proliferation and differentiation with cell-cycle regulation. However, the mechanisms coordinating these distinct cellular activities are poorly understood. Here we demonstrate for the first time that a Cut-like homeodomain transcription factor family member, Cux2 (Cutl2), regulates cell-cycle progression and development of neural progenitors. Cux2 loss-of-function mouse mutants exhibit smaller spinal cords with deficits in neural progenitor development as well as in neuroblast and interneuron differentiation. These defects correlate with reduced cell-cycle progression of neural progenitors coupled with diminished Neurod and p27(Kip1) activity. Conversely, in Cux2 gain-of-function transgenic mice, the spinal cord is enlarged in association with enhanced neuroblast formation and neuronal differentiation, particularly with respect to interneurons. Furthermore, Cux2 overexpression induces high levels of Neurod and p27(Kip1). Mechanistically, we discovered through chromatin immunoprecipitation assays that Cux2 binds both the Neurod and p27(Kip1) promoters in vivo, indicating that these interactions are direct. Our results therefore show that Cux2 functions at multiple levels during spinal cord neurogenesis. Cux2 initially influences cell-cycle progression in neural progenitors but subsequently makes additional inputs through Neurod and p27(Kip1) to regulate neuroblast formation, cell-cycle exit and cell-fate determination. Thus our work defines novel roles for Cux2 as a transcription factor that integrates cell-cycle progression with neural progenitor development during spinal cord neurogenesis.
| S-EPMC3093760 | biostudies-literature