Identification of glaikit in a genome-wide expression profiling for axonal bifurcation of the mushroom body in Drosophila
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE97607 | GEO | 2017/04/11
SECONDARY ACCESSION(S): PRJNA382401
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-02-03 | GSE94422 | GEO
Project description:Axonal branching is a fundamental requirement for sending electrical signals to multiple targets. However, despite the importance of axonal branching in neural development and function, the molecular mechanisms that control branch formation are poorly understood. Previous studies have hardly addressed the intracellular signaling cascade of axonal bifurcation characterized by growth cone splitting. Recently we reported that DISCO interacting protein 2 (DIP2) regulates bifurcation of mushroom body axons in Drosophila melanogaster. DIP2 mutant displays ectopic bifurcations in α/β neurons. Taking advantage of this phenomenon, we tried to identify genes involved in branching formation by comparing the transcriptome of wild type with that of DIP2 RNAi flies. A microarray analysis and a subsequent qRT-PCR experiment reviled that Glaikit (Gkt), a member of the phospholipase D (PLD) superfamily, is potentially a downstream target of DIP2. RNAi against gkt phenocopied the ectopic axonal branches observed in DIP2 mutant. Furthermore, a genetic analysis between gkt and DIP2 revealed that gkt acts in parallel with DIP2. In conclusion, we identified a novel gene underlying the axonal bifurcation process.
2017-02-03 | GSE94420 | GEO
Project description:Axonal branching is a fundamental requirement for sending electrical signals to multiple targets. However, despite the importance of axonal branching in neural development and function, the molecular mechanisms that control branch formation are poorly understood. Previous studies have hardly addressed the intracellular signaling cascade of axonal bifurcation characterized by growth cone splitting. Recently we reported that DISCO interacting protein 2 (DIP2) regulates bifurcation of mushroom body axons in Drosophila melanogaster. DIP2 mutant displays ectopic bifurcations in α/β neurons. Taking advantage of this phenomenon, we tried to identify genes involved in branching formation by comparing the transcriptome of wild type with that of DIP2 RNAi flies. A microarray analysis and a subsequent qRT-PCR experiment reviled that Glaikit (Gkt), a member of the phospholipase D (PLD) superfamily, is potentially a downstream target of DIP2. RNAi against gkt phenocopied the ectopic axonal branches observed in DIP2 mutant. Furthermore, a genetic analysis between gkt and DIP2 revealed that gkt acts in parallel with DIP2. In conclusion, we identified a novel gene underlying the axonal bifurcation process.
2017-02-03 | GSE94419 | GEO
Project description:Axonal branching is a fundamental requirement for sending electrical signals to multiple targets. However, despite the importance of axonal branching in neural development and function, the molecular mechanisms that control branch formation are poorly understood. Previous studies have hardly addressed the intracellular signaling cascade of axonal bifurcation characterized by growth cone splitting. Recently we reported that DISCO interacting protein 2 (DIP2) regulates bifurcation of mushroom body axons in Drosophila melanogaster. DIP2 mutant displays ectopic bifurcations in α/β neurons. Taking advantage of this phenomenon, we tried to identify genes involved in branching formation by comparing the transcriptome of wild type with that of DIP2 RNAi flies. After the microarray analysis, Glaikit (Gkt), a member of the phospholipase D superfamily, was identified as a downstream target of DIP2 by RNAi against gkt and qRT-PCR experiment. Single cell MARCM analysis of gkt mutant phenocopied the ectopic axonal branches observed in DIP2 mutant. Furthermore, a genetic analysis between gkt and DIP2 revealed that gkt potentially acts in parallel with DIP2. In conclusion, we identified a novel gene underlying the axonal bifurcation process.
2017-04-11 | GSE97606 | GEO
Project description:Axonal branching is a fundamental requirement for sending electrical signals to multiple targets. However, despite the importance of axonal branching in neural development and function, the molecular mechanisms that control branch formation are poorly understood. Previous studies have hardly addressed the intracellular signaling cascade of axonal bifurcation characterized by growth cone splitting. Recently we reported that DISCO interacting protein 2 (DIP2) regulates bifurcation of mushroom body axons in Drosophila melanogaster. DIP2 mutant displays ectopic bifurcations in α/β neurons. Taking advantage of this phenomenon, we tried to identify genes involved in branching formation by comparing the transcriptome of wild type with that of DIP2 RNAi flies. After the microarray analysis, Glaikit (Gkt), a member of the phospholipase D superfamily, was identified as a downstream target of DIP2 by RNAi against gkt and qRT-PCR experiment. Single cell MARCM analysis of gkt mutant phenocopied the ectopic axonal branches observed in DIP2 mutant. Furthermore, a genetic analysis between gkt and DIP2 revealed that gkt potentially acts in parallel with DIP2. In conclusion, we identified a novel gene underlying the axonal bifurcation process.
2017-04-11 | GSE97605 | GEO
Project description:Axonal branching is a fundamental requirement for sending electrical signals to multiple targets. However, despite the importance of axonal branching in neural development and function, the molecular mechanisms that control branch formation are poorly understood. Previous studies have hardly addressed the intracellular signaling cascade of axonal bifurcation characterized by growth cone splitting. Recently we reported that DISCO interacting protein 2 (DIP2) regulates bifurcation of mushroom body axons in Drosophila melanogaster. DIP2 mutant displays ectopic bifurcations in α/β neurons. Taking advantage of this phenomenon, we tried to identify genes involved in branching formation by comparing the transcriptome of wild type with that of DIP2 RNAi flies. After the microarray analysis, Glaikit (Gkt), a member of the phospholipase D superfamily, was identified as a downstream target of DIP2 by RNAi against gkt and qRT-PCR experiment. Single cell MARCM analysis of gkt mutant phenocopied the ectopic axonal branches observed in DIP2 mutant. Furthermore, a genetic analysis between gkt and DIP2 revealed that gkt potentially acts in parallel with DIP2. In conclusion, we identified a novel gene underlying the axonal bifurcation process.
2017-04-11 | GSE97604 | GEO
Project description:Identification of glaikit in a genome-wide expression profiling for axonal bifurcation of the mushroom body in Drosophila.
| PRJNA369656 | ENA
Project description:Identification of glaikit in a genome-wide expression profiling for axonal bifurcation of the mushroom body in Drosophila
| PRJNA382401 | ENA
Project description:Purpose: Exploring the alteration in CREB/CRTC binding related to long-term memory Methods: The nuclei of Drosophila mushroom bodies were purified and the histone acetylation and CREB/CRTC binding were examined by ChIP-seq using specific antibodies. The sequencing was performed using Miseq, and aligned to dm3 using CLCbio. The sequence reads that passed quality filters were analyzed by peak calling using PICS and ERD equipped on Strand NGS software. This method using two algorisms excludes false-positive calling of peaks. The PICS and ERD were run using a default setting except for the following parameters; for PICS, 120 bp as an average fragment length, 10 bp as a minimum distance between forward and reverse reads, 200 bp as a minimum distance between forward and reverse reads, 100 bp as a window width, with 5% false discovery rate; for ERD, 1.5 as an enrichment factor, 100 bp as a window size, 10 bp as a window slide size, 100 bp as a minimum region size. The peaks obtained by ERD analysis were filtered by an enrichment factor of 2, and a density of reads at 0.12 for CREB and 0.2 for CRTC. The CREB and the CRTC binding sites were determined as the peak-called region in at least 2 samples out of the three replicates. The CREB and the CRTC binding sites located 200 bp vicinity to each other were defined as the CREB/CRTC binding sites. In parallel, the read counts were obtained in the 1 kb window covering entire genome and analyzed by DESeq2, to determine the region enriched with CREB/CRTC in a specific group of samples. The region with increased or decreased CREB/CRTC binding were determined if the region were defined by the CREB/CRTC binding sites in the above criteria. Results: Using an optimized data analysis workflow, the filtered reads amounted to 8-11million reads for CREB in each of 3 replicates, 8-17 million reads for CRTC in each of 3 replicates, and 4.4 million reads for input. Using anti-CREB antibody, we found 239 significant increases in CREB binding out of 4995 CREB/CRTC binding sites 1 day after training. Using anti-CRTC antibody, we found 4989 significant increases in CRTC binding out of 4995 CREB/CRTC binding sites 1 day after spaced training. Conclusions: Our study shows that, although CREB binding is mostly unchanged, CRTC binding is significantly increased after long-term memory formation in Drosophila mushroom bodies.
2017-02-09 | GSE81456 | GEO
Project description:Nuclear receptors (NRs) comprise a family of ligand-regulated transcription factors that control diverse critical biological processes including various aspects of brain development. Eighteen NR genes exist in the Drosophila genome. To explore their roles in brain development, we knocked down individual NRs through the development of the mushroom bodies (MBs) by targeted RNAi. Besides recapitulating the known MB phenotypes for three NRs, we found that unfulfilled (unf), an ortholog of human photoreceptor specific nuclear receptor (PNR), regulates axonal morphogenesis and neuronal subtype identity. The adult MBs develop through remodeling of gamma neurons plus de-novo elaboration of both alpha'/beta' and alpha/beta neurons. Notably, unf is largely dispensable for the initial elaboration of gamma neurons, but plays an essential role in their re-extension of axons after pruning during early metamorphosis. The subsequently derived MB neuron types also require unf for extension of axons beyond the terminus of the pruned bundle. Tracing single axons revealed misrouting rather than simple truncation. Further, silencing unf in single-cell clones elicited misguidance of axons in otherwise unperturbed MBs. Such axon guidance defects may occur as MB neurons partially lose their subtype identity, as evidenced by suppression of various MB subtype markers in unf knockdown MBs. In sum, unf governs axonal morphogenesis of multiple MB neuron types, possibly through regulating neuronal subtype identity.
| S-EPMC2793019 | biostudies-literature