Perinatal correlated retinal activity is required for the wiring of visual axons in non-image forming nuclei
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA796364 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17567851.fastq.gz | Fastqsanger.gz | |||
| SRR17567852.fastq.gz | Fastqsanger.gz | |||
| SRR17567853.fastq.gz | Fastqsanger.gz | |||
| SRR17567854.fastq.gz | Fastqsanger.gz | |||
| SRR17567855.fastq.gz | Fastqsanger.gz |
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Project description:The formation of the visual system is a complex multistep process that includes the establishment of proper connectivity of retinal ganglion cell (RGC) axon terminals with their relay neurons located in the brain. In mammals, the assembly of the different components of the visual circuit occurs at perinatal stages before eye opening. Upon reaching the target nuclei RGC axons extensively arborize and subsequently refine to establish the final connections. Spontaneous activity generated in the immature retina plays an essential role in the refinement of visual terminals at the main image-forming nuclei (IFN) that follow an eye-specific and retinotopic organization. However, the molecular mechanisms underlying spontaneous activity-dependent axon remodeling, and the influence of this activity in the connectivity of non-image forming nuclei (NIFN) that lack precise retinotopic maps and/or eye-specific segregation, are not well known. Here, by generating conditional mice with disturbed spontaneous retinal aneactivity and analyzing their retinal transcriptomic profiles, we identified novel players involved in axon refinement at the visual nuclei (e. g. Syt13). The analysis of visual projections in the NIFN of these mice revealed that correlated-retinal activity shapes final connectivity in non retinotopic or eye-specific segregating visual nuclei.
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Project description:Local mRNA translation mediates the adaptive responses of axons to extrinsic signals but direct evidence that it occurs in mammalian CNS axons in vivo is scant. We developed an axon-TRAP-RiboTag approach in mouse that allows deep-sequencing analysis of ribosome-bound mRNAs in the retinal ganglion cell axons of the developing and adult retinotectal projection in vivo. The embryonic-to-postnatal axonal translatome comprises an evolving subset of enriched genes with axon-specific roles suggesting distinct steps in axon wiring, such as elongation, pruning and synaptogenesis. Adult axons, remarkably, have a complex translatome with strong links to axon survival, neurotransmission and neurodegenerative disease. Translationally co-regulated mRNA subsets share common upstream regulators, and novel sequence elements generated by alternative splicing that promote axonal mRNA translation. Our results indicate that intricate regulation of compartment-specific mRNA translation in mammalian CNS axons supports the formation and maintenance of neural circuits in vivo. The profiling of ribosome-bound mRNAs in mouse retinal ganglion cell axons at 4 different developmental stages
2016-06-16 | E-GEOD-79352 | biostudies-arrayexpress
Project description:Local mRNA translation mediates the adaptive responses of axons to extrinsic signals but direct evidence that it occurs in mammalian CNS axons in vivo is scant. We developed an axon-TRAP-RiboTag approach in mouse that allows deep-sequencing analysis of ribosome-bound mRNAs in the retinal ganglion cell axons of the developing and adult retinotectal projection in vivo. The embryonic-to-postnatal axonal translatome comprises an evolving subset of enriched genes with axon-specific roles suggesting distinct steps in axon wiring, such as elongation, pruning and synaptogenesis. Adult axons, remarkably, have a complex translatome with strong links to axon survival, neurotransmission and neurodegenerative disease. Translationally co-regulated mRNA subsets share common upstream regulators, and novel sequence elements generated by alternative splicing that promote axonal mRNA translation. Our results indicate that intricate regulation of compartment-specific mRNA translation in mammalian CNS axons supports the formation and maintenance of neural circuits in vivo.
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Project description:Loss-of-function mutations in chromatin remodeler gene ARID1A are a cause of Coffin-Siris syndrome, a developmental disorder characterized by dysgenesis of corpus callosum. Here, we characterize Arid1a function during cortical development and find unexpectedly selective roles for Arid1a in subplate neurons. Subplate neurons (SPNs), strategically positioned at the interface of cortical grey and white matter, orchestrate multiple developmental processes indispensable for neural circuit wiring. We find that pan-cortical deletion of Arid1a leads to extensive mistargeting of intracortical axons and agenesis of corpus callosum. Sparse Arid1a deletion, however, does not autonomously misroute callosal axons, implicating non-cell autonomous Arid1a functions in axon guidance. Supporting this possibility, the ascending axons of thalamocortical neurons, which are not autonomously affected by cortical Arid1a deletion, are also disrupted in their pathfinding into cortex and innervation of whisker barrels. Coincident with these miswiring phenotypes, which are reminiscent of subplate ablation, we unbiasedly find a selective loss of SPN gene expression following Arid1a deletion. In addition, multiple characteristics of SPNs crucial to their wiring functions, including subplate organization, subplate-thalamocortical axon co-fasciculation (“handshake”), and extracellular matrix, are severely disrupted. To empirically test Arid1a sufficiency in subplate, we generate a cortical plate deletion of Arid1a that spares SPNs. In this model, subplate Arid1a expression is sufficient for subplate-thalamocortical axon co-fasciculation and extracellular matrix assembly. Consistent with these wiring functions, subplate Arid1a sufficiently enables normal callosum formation, thalamocortical axon targeting, and whisker barrel development. Thus, Arid1a is a multifunctional regulator of subplate-dependent guidance mechanisms essential to cortical circuit wiring.
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Project description:Artificial intelligence has significantly advanced computational biology. Recent developments in omics technologies, such as single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST), provide detailed genomic data alongside tissue histology. However, current computational models often focus on either omics- or image-based analysis, lacking integration of both. To address this, we developed OmiCLIP, a visual-omics foundation model linking hematoxylin and eosin (H&E) images and transcriptomics using tissue patches from Visium data. For transcriptomics, we created 'sentences' by concatenating top-expressed gene symbols from tissue patches. We curated a dataset of 2.2 million paired tissue images and transcriptomic data across 32 organs to train OmiCLIP integrating histology and transcriptomics. Building on OmiCLIP, we created the Loki platform, which offers five key functions: tissue alignment, tissue annotation based on bulk RNA-seq or marker genes, cell type decomposition, image–transcriptomics retrieval, and ST gene expression prediction from H&E images. Compared with 22 state-of-the-art models on 5 simulations, 19 public, and 4 in-house experimental datasets, Loki demonstrated consistent accuracy and robustness in all tasks.
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Project description:The mechanisms controlling wiring of neuronal networks are not completely understood. The stereotypic architecture of the Drosophila mushroom-body (MB) offers a unique system to study circuit assembly. The adult medial MB γ-lobe is comprised of a long bundle of axons that wires with specific modulatory and output neurons in a tiled manner defining five distinct zones. We found that the immunoglobulin superfamily protein Dpr12 is cell-autonomously required in γ-neurons for their developmental regrowth into the distal γ4/5 zones, where both Dpr12 and its interacting protein, DIP-δ, are enriched. DIP-δ functions in a subset of dopaminergic neurons that wire with γ-neurons within the γ4/5 zone. During metamorphosis, these dopaminergic projections arrive to the γ4/5 zone prior to γ-axons, suggesting that γ-axons extend through a prepatterned region. Thus, Dpr12/DIP-δ transneuronal interaction is required for γ4/5 zone formation. Our study sheds light onto molecular and cellular mechanisms underlying circuit formation within subcellular resolution.
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Project description:Local protein synthesis is rapidly regulated by extrinsic signals during neural wiring but the translational control mechanisms remain elusive. Here, we show that the guidance cue Sema3A, but not Slit1, elicits precise spatiotemporal control of the phosphorylation of the translation initiation factor, eIF2α, in axonal growth cones via the Unfolded Protein Response (UPR) kinase PERK. Strikingly, in contrast to the canonical UPR signaling, we find that the Sema3A-induced eIF2α phosphorylation bypasses the conventional global translational repression and underlies a burst in axonal protein synthesis, mediated by differential eIF2B activity. Ultrasensitive proteomics on somaless axons reveals a subset of 75 proteins translationally regulated via Sema3A-p-eIF2α, including several proteostasis- and actin cytoskeleton-related nascent proteins. Finally, in vivo experiments provide evidence that eIF2α phosphorylation drives the formation of the retinotectal axon projection. Thus, specific extracellular cues can trigger non-canonical PERK-eIF2α-eIF2B signaling leading to subcellular dynamic remodeling of the nascent proteome required for neural wiring.
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