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Expression data from wildtype and mec-3 mutant PVD/OLL sensory neurons in C. elegans

ABSTRACT: 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).

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE46530 | GEO | 2013/05/02

SECONDARY ACCESSION(S): PRJNA200918

REPOSITORIES: GEO

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Expression data from wildtype and mec-3 mutant PVD/OLL sensory neurons in C. elegans

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

Expression data from the PVD and OLL neurons in C. elegans

2010-06-16 | GSE21162 | GEO

Expression data from the PVD and OLL neurons in C. elegans

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. We used expression arrays to identify genes highly enriched in the PVD neuron while undergoing dendritic morphogenesis. These genes could function in pathways controlling dendrite formation. We employ the mRNA-tagging method to isolate poly(A) RNA from the PVD and OLL neurons 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 gene expression microarrays. A reference sample was obtained by isolating total RNA from whole animals at the L3/L4 stages and processed as above.

2010-07-08 | E-GEOD-21162 | biostudies-arrayexpress

Dynamic Gene Expression Response to TGF-β Stimulation in Multipotent Progenitors and Common Dendritic Cell Progenitors

Project description:Multipotent progenitors (MPP) and common dendritic cell progenitors (CDP) were obtained from mouse bone marrow, followed by in vitro culture with a specific cytokine cocktail and FACS sorting (Felker et al., 2010; Seré et al., 2012). Cells were treated with 10 ng/ml recombinant human TGF-β1 (R&D Systems, Minneapolis, USA) for 2, 4, 8, 12 and 24 h as described (Felker et al., 2010) or left untreated.

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Project description:We have quantified gene expression in five tissues (brain, heart, kidney, liver and testis) from humans, chimpanzees and rhesus macaques using the Illumina NlaIII Digital Gene Expression (DGE) protocol. This dataset extends a previous microarray study by Khaitovich et al. (Khaitovich et al. 2005) with the rhesus macaque outgroup and complements other previously generated tissue transcriptome profiles from primates (Enard et al. 2002; Khaitovich et al. 2006; Somel et al. 2009; Babbitt et al. 2010; Blekhman et al. 2010; Wetterbom et al. 2010). contributor: Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, D-04103 Leipzig, Germany

2013-10-01 | GSE50782 | GEO

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Project description:MEC-sludge Genome sequencing

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Project description:The potential involvement of PI3Kγ in immune-related diseases has been recently investigated leading to efforts in developing specific inhibitors of this isoform as therapeutic strategies. (Takeda et al 2010, Rommel et al 2007). Of particular significance to cutaneous disease, murine studies have indicated the importance of PI3Kγ in Langerhans cell (LC) function. Recently, it has been postulated, PI3Kγ is a molecular switch that controls immune suppression in macrophages, a cell type closely related to LCs. [Nature letter 2016]. In our analysis PIK3CG, encoding PI3Kγ was highly expressed by LC, in contrast to dermal dendritic cells (Polak et al 2014). Here we sought to examine the effect of PI3Kg inhibition on the function of human epidermal LCs.

2017-03-30 | GSE94247 | GEO

Transcriptomic characterization of in vitro human iPSC-derived motor neuron systems for the exploration of cell autonomous mechanisms and modifiers of TDP-43 perturbation associated neurotoxicity

Project description:Transactive Response DNA-binding protein 43 (TDP-43) is a multifunctional nuclear protein ubiquitously expressed in all tissues. Although it is primarily nuclear, Amyotrophic Lateral Sclerosis (ALS) patients frequently present with cytoplasmic aggregates of TDP-43 in motor neurons on post-mortem examination. Although only about 5% of all ALS patients have a TARDBP mutation (Ghasemi and Brown 2018; Ingre et al. 2015), which is known to cause these insoluble cytoplasmic aggregates, 97% of ALS patients will develop cytoplasmic, insoluble TDP-43 aggregates regardless of whether they have a mutation in TARDBP or not (Ling et al. 2013). Overexpression of wild-type TDP-43 has previously been shown to be a valid model of inducing neurotoxicity as well as a limited amount of cytoplasmic re-localization and aggregation characteristic of ALS (Elden et al. 2010; Wils et al. 2010). In the search for modifiers of toxicity as conferred by TDP-43 overexpression in these models, knockout of Ataxin-2 (ATXN2) was proposed as a protective intervention in the context of TDP-43 perturbation in non-human model systems (Elden et al. 2010, Becker et al. 2017). This promising finding had not previously been validated in a human motor neuron system, nor had a thorough investigation been conducted to determine the mechanism of neuroprotection that ATXN2 knockout employs to drive the therapeutic effect. This sequencing study examines both ATXN2 intact and ATXN2 knockout motor neurons in the context of TDP-43 perturbation to explore global transcriptomic changes that arise from these changes in cellular state that are associated with progression of ALS (ATXN2 intact) and what pathways could be implicated in protection from ALS-associated neurodegeneration (ATXN2 Knockout).

2024-03-23 | GSE261875 | GEO

RNA-seq analysis of differences in gene expression between dorsal and ventral MEC

Project description:Neural circuits in the medial entorhinal cortex (MEC) encode an animal’s position and orientation in space. Within the MEC spatial representations, including grid and directional firing fields, have a laminar and dorsoventral organization that corresponds to a similar topography of neuronal connectivity and cellular properties. Yet, in part due to the challenges of integrating anatomical data at the resolution of cortical layers and borders, we know little about the molecular components underlying this organization. To address this we develop a new computational pipeline for high-throughput analysis and comparison of in situ hybridization (ISH) images at laminar resolution. We apply this pipeline to ISH data for over 16,000 genes in the Allen Brain Atlas and validate our analysis with RNA sequencing of MEC tissue from adult mice. We find that differential gene expression delineates the borders of the MEC with neighboring brain structures and reveals its laminar and dorsoventral organization. Our analysis identifies ion channel-, cell adhesion- and synapse-related genes as candidates for functional differentiation of MEC layers and for encoding of spatial information at different scales along the dorsoventral axis of the MEC. Our results support the hypothesis that differences in gene expression contribute to functional specialization of superficial layers of the MEC and dorsoventral organization of the scale of spatial representations.

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