MRNAseq of wild type and ets-5 mutant C. elegans BAG neurons
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ABSTRACT:
PROVIDER: PRJNA680272 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13111086_1.fastq.gz | Fastqsanger.gz | |||
| SRR13111086_2.fastq.gz | Fastqsanger.gz | |||
| SRR13111087_1.fastq.gz | Fastqsanger.gz | |||
| SRR13111087_2.fastq.gz | Fastqsanger.gz | |||
| SRR13111088_1.fastq.gz | Fastqsanger.gz |
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Project description:comparative transcriptomics of wild type and ets-5 mutant C. elegans BAG neurons
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Project description:The extent to which behavior is shaped by experience varies between individuals. Genetic differences contribute to this variation but the neural mechanisms are not understood. In this study, we identify a natural genetic variant of the dendritic scaffolding protein ARCP-1 that modifies individual behavioral flexibility in C. elegans. Disrupting ARCP-1 alters how previous oxygen experience modulates escape behavior in response to carbon dioxide. ARCP-1 normally suppresses CO2 aversion by inhibiting signaling from the BAG CO2-sensing neurons. To further investigate how disrupting ARCP-1 alters BAG function, we specifically labeled these neurons with GFP, used FACS to isolate the fluorescent cells from acutely dissociated arcp-1 mutant and control animals, and profiled their gene expression using RNA-Seq. We find transcriptional changes for a broad range of gene classes and link altered neuropeptide expression to increased CO2 aversion in the arcp-1 mutant.
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Project description:Purpose: The goals of this study are to identify cellular pathways to recover a-syn aggregation-mediated toxicity induced in response to CDC or BAG treatment on PD-iPSC derived mDA neurons. Methods: mRNA profiles of 30-day-old PD-mDA neurons with CDC or BAG treatment for 1 day were generated by deep sequencing, in duplicate, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Conclusions: Our study represents the detailed analysis of mDA neuronal transcriptomes in response to CDC or BAG treatments, with biologic replicates, generated by RNA-seq technology. Our results show that CDC or BAG treatment could rescue the toxcity from a-syn aggregation via purine metabolism / ion transport pathways.
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Project description:The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals
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Project description:RNA-seq profiling of BAG neurons in C. elegans npr-1 and npr-1 arcp-1 animals
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Project description:The nervous system comprises diverse and highly specialized neuron-types, each expressing a unique set of genes that defines its functional properties. What molecular mechanisms generate diverse neuron types remains a central question in neuroscience. Our study of C. elegans chemosensory BAG neurons showed that a p38 MAP kinase (MAPK), PMK-3, is required for their proper differentiation and function (Brandt, J. and Ringstad, N. 2015). How p38 MAPKs function in neurodifferentiation is poorly understood. To better understand how pmk-3 promotes the BAG cell fate, we purified wild-type and pmk-3 mutant chemosensory BAG neurons and determined their transcriptomes using RNA-Seq. Expression of a number of genes that encode neuropeptides, including insulin-like peptides (ILPs), were up-regulated in pmk-3 mutant BAG neurons. Through analysis of mutations that restore expression of a BAG-fate marker to pmk-3 mutants, we additionally found that genes required for the release of neuropeptides, including UNC-31/CAPS, suppress pmk-3 mutant gene expression defects. These two observations suggested that the differentiation defects of pmk-3 mutants are associated with dysregulated release of peptide hormones. Indeed, we find that increased synthesis and release of ILPs from BAG during development causes a significant fraction of the gene expression and functional defects of pmk-3 mutant neurons. Together our data delineate a mechanism through which p38 MAPKs promote proper sensory neuron differentiation by inhibiting an autocrine insulin signal that represses expression of a BAG neuron fate. These findings reveal an unexpected role for insulin signaling in nervous system development and suggest that insulin-like factors are at the nexus of intrinsic genetic programs and extrinsic signaling mechanisms that regulate cell fate and neuronal differentiation.
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Project description:Next Generation Sequencing of PD-iPSC derived midbrain dopaminergic(mDA) neurons treated with CDC (C021 dihychloride) or BAG (BAG 956)
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Project description:Background: Differential gene expression specifies the highly diverse cell types that constitute the nervous system. With its sequenced genome and simple, well-defined neuroanatomy, the nematode C. elegans is a useful model system in which to correlate gene expression with neuron identity. The UNC-4 transcription factor is expressed in thirteen embryonic motor neurons where it specifies axonal morphology and synaptic function. These cells can be marked with an unc-4::GFP reporter transgene. Here we describe a powerful strategy, Micro-Array Profiling of C. elegans cells (MAPCeL), and confirm that this approach provides a comprehensive gene expression profile of unc-4::GFP motor neurons in vivo. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate unc-4::GFP neurons from primary cultures of C. elegans embryonic cells. Microarray experiments detected 6,217 unique transcripts of which ~1,000 are enriched in unc-4::GFP neurons relative to the average nematode embryonic cell. The reliability of these data was validated by the detection of known cell-specific transcripts and by expression in UNC-4 motor neurons of GFP reporters derived from the enriched data set. In addition to genes involved in neurotransmitter packaging and release, the microarray data include transcripts for receptors to a remarkably wide variety of signaling molecules. The added presence of a robust array of G-protein pathway components is indicative of complex and highly integrated mechanisms for modulating motor neuron activity. Over half of the enriched genes (537) have human homologs, a finding that could reflect substantial overlap with the gene expression repertoire of mammalian motor neurons. Conclusion: We have described a microarray-based method, MAPCeL, for profiling gene expression in specific C. elegans motor neurons and provide evidence that this approach can reveal candidate genes for key roles in the differentiation and function of these cells. These methods can now be applied to generate a gene expression map of the C. elegans nervous system. Experiment Overall Design: Our goal is to profile gene expression throughout the nervous system of the model organism Caenorhabditis elegans. As a first goal, we profiled a single class of embryonic motor neurons. To isolate transcripts from thesec neurons we developed the MAPCeL (Microarray Profiling C. elegans Cells) technique in which unc-4::GFP+ cells are captured by FACS for RNA isolation. We verified these data by bioinformatic means and by in vivo validation by creating GFP reporters for a random set of genes in our enriched gene list.
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