Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA270933 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1729340.fastq.gz | Fastqsanger.gz | |||
| SRR1729341.fastq.gz | Fastqsanger.gz | |||
| SRR1729333.fastq.gz | Fastqsanger.gz | |||
| SRR1729334.fastq.gz | Fastqsanger.gz | |||
| SRR1729335.fastq.gz | Fastqsanger.gz |
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Project description:Pediatric neural tumors are initiated during embryonic/fetal stages and rapidly become malignant despite carrying few genetic alterations. However, the molecular basis of this early malignant susceptibility remains unknown. During Drosophila development, malignant neural tumors can arise from single gene inactivation triggering dedifferentiation towards a neural stem cell (NSC)-like state. Here, we find that these tumors originate from a sub-population of early-born neural progeny that transiently co-express the mRNA-binding proteins Lin-28 and Imp/IGF2BP, and the transcription factor Chinmo. These three genes compose an early growth module that is co-opted in a subset of dedifferentiated cells to propagate unlimited proliferation. In late NSCs, Chinmo, Imp and Lin-28 are silenced by temporal transcription factors for timely termination of neurogenesis. Consequently, late-born progeny do not express the module and become refractory to malignant transformation. Thus, this study identifies the NSC-intrinsic developmental program that predisposes neural progeny to malignant transformation according to their birth order.
2017-02-09 | GSE64405 | GEO
Project description:The vertebrate neural tube generates a large diversity of molecularly and functionally distinct neurons and glia from a small progenitor pool. While the role of spatial patterning in organising cell fate specification has been extensively studied, temporal patterning, which controls the timing of cell type generation, is equally important. Here we define a global temporal programme in the spinal cord. This governs cell fate choices by regulating chromatin accessibility in neural progenitors. Perturbation of this cis-regulatory programme affects sequential transitions in spinal cord progenitors and the identity of progeny. The temporal programme operates in parallel to spatial patterning, ensuring the timely availability of regulatory elements for spatial determinants to direct cell-type specific gene expression. These findings identify a chronotopic spatiotemporal integration strategy in which a global temporal chromatin programme determines the output of a spatial gene regulatory network resulting in the temporally and spatially ordered allocation of cell type identity.
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Project description:The vertebrate neural tube generates a large diversity of molecularly and functionally distinct neurons and glia from a small progenitor pool. While the role of spatial patterning in organising cell fate specification has been extensively studied, temporal patterning, which controls the timing of cell type generation, is equally important. Here we define a global temporal programme in the spinal cord. This governs cell fate choices by regulating chromatin accessibility in neural progenitors. Perturbation of this cis-regulatory programme affects sequential transitions in spinal cord progenitors and the identity of progeny. The temporal programme operates in parallel to spatial patterning, ensuring the timely availability of regulatory elements for spatial determinants to direct cell-type specific gene expression. These findings identify a chronotopic spatiotemporal integration strategy in which a global temporal chromatin programme determines the output of a spatial gene regulatory network resulting in the temporally and spatially ordered allocation of cell type identity.
2024-04-22 | GSE264170 | GEO
Project description:The vertebrate neural tube generates a large diversity of molecularly and functionally distinct neurons and glia from a small progenitor pool. While the role of spatial patterning in organising cell fate specification has been extensively studied, temporal patterning, which controls the timing of cell type generation, is equally important. Here we define a global temporal programme in the spinal cord. This governs cell fate choices by regulating chromatin accessibility in neural progenitors. Perturbation of this cis-regulatory programme affects sequential transitions in spinal cord progenitors and the identity of progeny. The temporal programme operates in parallel to spatial patterning, ensuring the timely availability of regulatory elements for spatial determinants to direct cell-type specific gene expression. These findings identify a chronotopic spatiotemporal integration strategy in which a global temporal chromatin programme determines the output of a spatial gene regulatory network resulting in the temporally and spatially ordered allocation of cell type identity.
2024-04-23 | GSE264637 | GEO
Project description:The vertebrate neural tube generates a large diversity of molecularly and functionally distinct neurons and glia from a small progenitor pool. While the role of spatial patterning in organising cell fate specification has been extensively studied, temporal patterning, which controls the timing of cell type generation, is equally important. Here we define a global temporal programme in the spinal cord. This governs cell fate choices by regulating chromatin accessibility in neural progenitors. Perturbation of this cis-regulatory programme affects sequential transitions in spinal cord progenitors and the identity of progeny. The temporal programme operates in parallel to spatial patterning, ensuring the timely availability of regulatory elements for spatial determinants to direct cell-type specific gene expression. These findings identify a chronotopic spatiotemporal integration strategy in which a global temporal chromatin programme determines the output of a spatial gene regulatory network resulting in the temporally and spatially ordered allocation of cell type identity.
2024-04-22 | GSE264149 | GEO
Project description:During development, neural stem cells are temporally patterned to sequentially generate a variety of neural types before exiting the cell cycle. Temporal patterning is well-studied in Drosophila, where neural stem cells called neuroblasts sequentially express cascades of Temporal Transcription Factors (TTFs) to control the birth-order dependent neural specification. However, currently known TTFs were mostly identified through candidate antibody screening and may not be complete. In addition, many fundamental questions remain concerning the TTF cascade initiation, progression, and termination. It is also not known why temporal progression only happens in neuroblasts but not in their differentiated progeny. In this work, we performed single-cell RNA sequencing of Drosophila medulla neuroblasts of all ages to study the temporal patterning process with single-cell resolution. Our scRNA-seq data revealed that sets of genes involved in different biological processes show high to low or low to high gradients as neuroblasts age. We also identified a list of novel TTFs, and experimentally characterized their roles in the temporal progression and neural fate specification. Our study revealed a comprehensive temporal gene network that patterns medulla neuroblasts from start to end. Furthermore, we found that the progression and termination of this temporal cascade also require transcription factors differentially expressed along the differentiation axis (neuroblasts -> -> neurons). Lola proteins function as a speed modulator of temporal progression in neuroblasts; while Nerfin-1, a factor required to suppress de-differentiation in post-mitotic neurons, acts at the final temporal stage together with the last TTF of the cascade, to promote the switch to gliogenesis and the cell cycle exit. Our comprehensive study of the medulla neuroblast temporal cascade illustrated mechanisms that might be conserved in the temporal patterning of neural stem cells.
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Project description:One neural stem cell can produce multiple transiently amplifying, intermediate neural progenitors (INP), which collectively yield diverse neuronal types. It is unclear if and how serially derived INPs contribute to neuron fate diversification. Drosophila type II neuroblasts, like mammalian neural stem cells, deposit neurons and also glia through INPs. The consecutively born INPs in a given lineage produce morphologically distinct progeny, presumably due to their inheritance of different temporal factors from the INP-producing progenitor. To uncover the underlying temporal fating mechanisms, we profiled type II neuroblasts' transcriptome across time. Our results reveal opposing temporal gradients of Imp and Syp RNA-binding proteins (descending and ascending, respectively). Maintaining high Imp throughout serial INP production expands the number of neurons/glia with early temporal fate at the expense of cells with late fate. Conversely, precocious upregulation of Syp reduces the number of cells with early fate. Further, we reveal that the transcription factor, Seven-up initiates progression of the Imp/Syp gradients. Interestingly, neuroblasts apparently locked in their beginning Imp/Syp levels can still yield progeny with a small range of early fates. We propose that the Seven-up-initiated Imp/Syp gradients create coarse temporal windows within type II neuroblasts to pattern INPs, which subsequently undergo fine-tuned subtemporal patterning.
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Project description:The Notch pathway is a well conserved cell to cell communication mechanism that is normally involved in many developmental processes and when aberrantly activated it leads to diseases such as cancer. One such example is the neural stem cell tumours that arise from constitutive Notch activity in Drosophila neuroblasts from the larval Central Nervous System (CNS). To investigate how hyper-activation of Notch in larval neuroblasts leads to tumours, we mapped genome-widely the regions that are bound by Su(H) (the core Notch pathway transcription factor, known as CSL in mammals). We combined these results with the profiling of upregulated mRNAs in CNSs where Notch is hyper-activated for 24h vs control CNSs and identified 127 putative direct Notch targets in the hyperplastic CNSs. Included were genes associated with the neuroblast maintenance and self-renewal programme and genes coding for temporal transcription factors, which are involved in neuroblast progression and generation of progeny with specific identity over time. Thus, Notch induces neural stem cell tumors by promoting the expression of genes that contribute to stem cell identity and by reprogramming expression of temporal factors that regulate maturity. Su(H) binding profile in Drosophila larval CNSs where Notch is constitutively active for 24 hours. In total there are 3 samples of Su(H) ChIP in Notch hyper-activated larval CNSs.
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Project description:Neural stem cells (NSCs) generate highly diverse neurons over time by acquiring new features, a phenomenon called as temporal patterning. However the mechanisms underlying temporal patterning still remains poorly understood. Here, we describe a method that allows to isolate different temporal stages of Drosophila transit amplifying cells called intermediate neural porgenitors (INPs). We identified odd-paired (opa) as the regulator of the transition from first to second temporal stages, which are defined by D and Grh expression. We demonstrated that opa is required for correct neural output and brain morphology. We showed that opa achieves this transition via repressing D. Together with upstream SWI/SNF complex, D and opa forms an incoheren feed forward loop, which results in successive expression of temporal identities.
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Project description:The Notch pathway is a well conserved cell to cell communication mechanism that is normally involved in many developmental processes and when aberrantly activated it leads to diseases such as cancer. One such example is the neural stem cell tumours that arise from constitutive Notch activity in Drosophila neuroblasts from the larval Central Nervous System (CNS). To investigate how hyper-activation of Notch in larval neuroblasts leads to tumours, we mapped genome-widely the regions that are bound by Su(H) (the core Notch pathway transcription factor, known as CSL in mammals). We combined these results with the profiling of upregulated mRNAs in CNSs where Notch is hyper-activated for 24h vs control CNSs and identified 127 putative direct Notch targets in the hyperplastic CNSs. Included were genes associated with the neuroblast maintenance and self-renewal programme and genes coding for temporal transcription factors, which are involved in neuroblast progression and generation of progeny with specific identity over time. Thus, Notch induces neural stem cell tumors by promoting the expression of genes that contribute to stem cell identity and by reprogramming expression of temporal factors that regulate maturity.
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