Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Branching Gene Regulatory Network for Neurotransmitter versus Axonal Pathfinding

ABSTRACT: In previous studies we found that the two transcription factors collier (FB:knot, kn) [vertebrate Ebf1] and ladybird early (lbe) [vertebrate Lbx1/2], when co-misexpressed from elav-Gal4, generate ectopic Nplp1 neuropeptidergic cells in the entire ventral nerve cord during Dmel. embryonic development. We also found that the axon generated by the ectopic Nplp1 cells, seem to follow the same fascicle as the wild type Nplp1 neurons. Therefore we used RNA-seq on control and UAS‑col,lbe co-misexpression to find candidate factors important in axon pathfinding of the Nplp1 neurons. We also included single misexpression of UAS-col and UAS-lbe, together with co-misexpression of UAS-ap, eya, since we know that col and lbe activate those two factors during the cell fate specification of Nplp1 neurons.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE113260 | GEO | 2019/03/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional and splicing response of two Arabidopsis thaliana natural accessions to ABA-mediated stress.

Project description:RNA-seq experiment to study the transcriptional and splicing changes of two Arabidopsis thaliana natural accessions, Col-0 and Kn-0, grown for 4 days under normal conditions and transferred to control medium or 5 µM ABA for 3 hours.

2023-11-06 | GSE228303 | GEO

Expression profiling of isolated dendritic arborization (da) neurons of Drosophila

Project description:Paper abstract: The transcription factors Abrupt (Ab) and Knot (Kn) act as selectors of distinct dendritic arbor morphologies in two classes of Drosophila sensory neurons, termed class I and class IV, respectively. We performed binding-site mapping and transcriptional profiling of isolated these neurons. Their profiles were similarly enriched in cell-type-specific enhancers of genes implicated in neural development. We identified a total of 429 target genes, of which 56 were common to Ab and Kn; these targets included genes necessary to shape dendritic arbors in either or both of the two sensory subtypes. Furthermore, a common target gene, encoding the cell adhesion molecule Ten-m, was expressed more strongly in class I than IV, and this differential was critical to the class-selective directional control of dendritic branch sprouting or extension. Our analyses illustrate how differentiating neurons employ distinct and shared repertoires of gene expression to produce class-selective morphological traits. da neurons were isolated by magnetic bead sorting from larvae of the following three genotypes and obtained genome-wide expression profiles: larvae expressing a cell-surface marker mCD8:GFP alone (Control), and larvae ectopically expressing Abrupt (Ab ME) or Knot (Kn ME) together with mCD8:GFP in all classes of da neurons. 3 biological replicates were collected.

2013-11-27 | E-GEOD-38660 | biostudies-arrayexpress

Drosophila egg chambers: control vs. ectopic JAK/STAT and EGFR signaling

Project description:During Drosophila melanogaster oogenesis, the JAK/STAT and EGFR pathways are both required to specify a population of somatic epithelial cells called the posterior follicle cells (PFCs). The PFCs are important because they generate a signal at mid-oogenesis that is required to establish the embryonic axes. To identify novel PFC-expressed transcripts, egg chambers containing ectopic PFCs were generated and microarrays were then used to identify upregulated transcripts. To generate ectopic PFCs, GAL80TS / CyO ; UAS-Upd, UAS-λtorpedo/TM6B flies were crossed to GR1-GAL4 flies to obtain the genotype GAL80TS/+ ; GR1-GAL4/UAS-Unpaired, UAS-λtorpedo. Sibling females of genotype GAL80TS/+ ; GR1-GAL4/TM6B were dissected as controls.

2018-10-30 | GSE118881 | GEO

Single-cell RNA-seq data for control and POU IV-misexpressed Ciona intestinalis embryos at late tailbud (LTB) stage

Project description:Purpose: Understand how the misexpression of key sensory cell determinant POU IV affects cell type specification of various sensory neurons in the peripheral nervous system in Ciona. Methods: CesA>POU IV (2.5ng/l) + CesA>GFP (5.0ng/l) injected eggs and control eggs were fertilized side by side, and allowed to develop to the late tailbud stage (13.5h after fertilization at 18°C). For each sample, 120 morphologically normal embryos were used for single cell RNA-seq assays. Dissociation of the embryos and single cell RNA-seq assays by 10x Genomics chromium system were done as described in 9. Horie R. et al., Shared evolutionary origin of vertebrate neural crest and cranial placodes. Nature 560, 228-232 (2018). Results: Misexpression of POU IV leads to the formation of Synthetic Cell Types that exhibit properties of other sensory neurons, especially those of bipolar tail neurons (BTNs) and a synthetic gene battery that is not found in any wildtype sensory neuron.

2021-12-29 | GSE192645 | GEO

RNA-sequencing of Drosophila expressing mutant Huntingtin in neurons or glia

Project description:We performed RNA-seq on head tissue collected from Drosophila expressing N-terminal (UAS-HTTNT231Q128) or full-length (UAS-HTTFL200Q) human mHTT in neurons (elav-GAL4) or glia (repo-GAL4).

2021-06-03 | GSE157287 | GEO

Expression profiling of isolated dendritic arborization (da) neurons of Drosophila

2013-11-27 | GSE38660 | GEO

DamID profiling of neural transcription factor (Abrupt and Knot) binding in Drosophila melanogaster embryos

2013-11-27 | GSE38659 | GEO

Expression data from embryonic mouse cervical spinal cords

Project description:Mammalian motor circuits control voluntary movements by transmitting signals from the central nervous system (CNS) to muscle targets. To form these circuits, motor neurons (MNs) must extend their axons out of the CNS. Although motor axon exit from the CNS is an indispensable phase of motor axon pathfinding, the underlying molecular mechanisms remain obscure. Here, we present the first identification of a genetic pathway that¬†regulates motor axon exit from the vertebrate spinal cord, utilizing spinal accessory motor neurons (SACMN) as a model system. SACMN are a homogeneous population of spinal MNs whose axons leave the CNS through a discrete lateral exit point (LEP) and can be visualized by the expression of the cell surface protein, BEN. We show that the homeodomain transcription factor, Nkx2.9, is selectively required for SACMN axon exit and identify the Robo2 guidance receptor as a likely downstream effector of Nkx2.9; loss of Nkx2.9 leads to a reduction in Robo2 mRNA and protein within SACMN and SACMN axons fail to exit the spinal cord in Robo2-deficient mice. Consistent with short-range interactions between Robo2 and Slit ligands regulating SACMN axon exit, Robo2-expressing SACMN axons normally navigate through LEP-associated Slits as they emerge from the spinal cord, and fail to exit in Slit-deficient mice. Our studies support the view that Nkx2.9 controls SACMN axon exit from the mammalian spinal cord by regulating Robo-Slit signaling. We utilized microarray technology to identify novel downstream effectors of the homeodomain transcription factor, Nkx2.9, that regulate spinal accessory motor neuron development.

2013-06-15 | E-GEOD-47953 | biostudies-arrayexpress

DamID profiling of neural transcription factor (Abrupt and Knot) binding in Drosophila melanogaster embryos

Project description:Paper abstract: The transcription factors Abrupt (Ab) and Knot (Kn) act as selectors of distinct dendritic arbor morphologies in two classes of Drosophila sensory neurons, termed class I and class IV, respectively. We performed binding-site mapping and transcriptional profiling of isolated these neurons. Their profiles were similarly enriched in cell-type-specific enhancers of genes implicated in neural development. We identified a total of 429 target genes, of which 56 were common to Ab and Kn; these targets included genes necessary to shape dendritic arbors in either or both of the two sensory subtypes. Furthermore, a common target gene, encoding the cell adhesion molecule Ten-m, was expressed more strongly in class I than IV, and this differential was critical to the class-selective directional control of dendritic branch sprouting or extension. Our analyses illustrate how differentiating neurons employ distinct and shared repertoires of gene expression to produce class-selective morphological traits. Each Dam-fusion-derived sample is compared to a control Dam-only sample. Four biological replicates were performed.

2013-11-27 | E-GEOD-38659 | biostudies-arrayexpress

Expression data from embryonic mouse cervical spinal cords

Project description:Mammalian motor circuits control voluntary movements by transmitting signals from the central nervous system (CNS) to muscle targets. To form these circuits, motor neurons (MNs) must extend their axons out of the CNS. Although motor axon exit from the CNS is an indispensable phase of motor axon pathfinding, the underlying molecular mechanisms remain obscure. Here, we present the first identification of a genetic pathway that regulates motor axon exit from the vertebrate spinal cord, utilizing spinal accessory motor neurons (SACMN) as a model system. SACMN are a homogeneous population of spinal MNs whose axons leave the CNS through a discrete lateral exit point (LEP) and can be visualized by the expression of the cell surface protein, BEN. We show that the homeodomain transcription factor, Nkx2.9, is selectively required for SACMN axon exit and identify the Robo2 guidance receptor as a likely downstream effector of Nkx2.9; loss of Nkx2.9 leads to a reduction in Robo2 mRNA and protein within SACMN and SACMN axons fail to exit the spinal cord in Robo2-deficient mice. Consistent with short-range interactions between Robo2 and Slit ligands regulating SACMN axon exit, Robo2-expressing SACMN axons normally navigate through LEP-associated Slits as they emerge from the spinal cord, and fail to exit in Slit-deficient mice. Our studies support the view that Nkx2.9 controls SACMN axon exit from the mammalian spinal cord by regulating Robo-Slit signaling.

2013-06-15 | GSE47953 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data