Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA200918 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. MEC-3 is a transcription factor expressed in the PVD neuron (Chatzigeorgiou et al., 2010; Li et al., 2011; Way and Chalfie, 1989). mec- 3 mutant PVD neurons fail to elaborate lateral branches and show defective function (Smith et al., 2010; Tsalik et al., 2003) (Husson et al., 2012). We used tiling arrays to identify genes regulated by the mec-3 transcription factor in PVD sensory neurons. We employ the mRNA-tagging method to isolate poly(A) RNA from the PVD and OLL neurons in wildtype and mec-3 mutants (3 replicates each) by expressing a 3X FLAG-tagged poly(A) binding protein PAB-1 in PVD and OLL under control of the ser-2prom3B promoter. The enriched poly(A) RNA is amplified using the NuGEN WT-Pico amplification system and applied to Affymetrix C. elegans tiling microarrays. Whole animal reference samples were obtained by isolating total RNA at the L2/L3 stages in wildtype and mec-3 mutants (2 replicates each) and processed as above.
2013-05-02 | E-GEOD-46530 | biostudies-arrayexpress
Project description:Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans
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Project description:Expression data from wildtype and gas-1 mitochondrial mutant C. elegans
| PRJNA105143 | ENA
Project description:Nociceptive neurons develop a complex dendritic arbor to sense noxious stimuli, which enables animals to react to environmental insults and perform self-protective behaviours. The genetic programs controlling neuronal dendritic morphogenesis are poorly understood. In C. elegans, the PVD sensory neuron generates a complex dendritic arbor that envelops the body of the animal. This nociceptive neuron enables study of dendrite formation in vivo. MEC-3 is a transcription factor expressed in the PVD neuron (Chatzigeorgiou et al., 2010; Li et al., 2011; Way and Chalfie, 1989). mec- 3 mutant PVD neurons fail to elaborate lateral branches and show defective function (Smith et al., 2010; Tsalik et al., 2003) (Husson et al., 2012).
2013-05-02 | GSE46530 | GEO
Project description:We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells. Affymetrix gene expression data from isolated populations of mir-124 expressing (GFP+) and non-expressing (GFP-) cells obtained from wild-type and mir-124 mutant C. elegans (in biological triplicates)
2010-03-22 | E-GEOD-16050 | biostudies-arrayexpress
Project description:Expression data from 2 wildtype and 8 C. elegans ETC mutants
| PRJNA105145 | ENA
Project description:Comparison of gene expression profiles from C. elegans mutant strains (MIR73, MIR75 or MIR77) overexpressing genes involved in proline metabolism (B0513.5 or T22H6.2) with wildtype strain (N2) at 5 days after L4 larvae stage. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
2021-10-19 | GSE110842 | GEO
Project description:Expression data from the PVD and OLL neurons in C. elegans
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Project description:Single-cell RNA-seq of PLM, AFD, and ASER sensory neurons of Caenorhabditis elegans.
| PRJNA320925 | ENA
Project description:Abstract: Animals that lose one sensory modality often show augmented responses to other sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly understood. To probe these mechanisms, we perform a forward genetic screen for mutants with enhanced O2 perception in C. elegans. Multiple mutants exhibiting increased responsiveness to O2 concomitantly show defects in other sensory responses. One mutant, qui-1, defective in a conserved NACHT/WD40 protein, abolishes pheromone-evoked Ca2+ responses in the ADL chemosensory neurons. We find that ADL’s responsiveness to pre-synaptic input from O2-sensing neurons is heightened in qui-1 and other sensory defective mutants resulting in an enhanced neurosecretion. Expressing qui-1 selectively in ADL rescues both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. Profiling of ADL neurons indicates its acquired O2-evoked neurosecretion is the result of a transcriptional reprogramming that up-regulates neuropeptide signalling. We show that the conserved neuropeptide receptor NPR-22 is necessary and sufficient in ADL to enhance its neurosecretion levels. Sensory loss can thus confer cross-modal plasticity by re-wiring peptidergic circuits.
2021-03-10 | GSE168597 | GEO