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RNA-seq: Transcriptome profile between wild type control and Alk-YS mutant in the Drosophila larval CNS.

ABSTRACT: RNA-seq: Transcriptome profile between wild type control and Alk-YS mutant in the Drosophila larval CNS.

PROVIDER: PRJNA816924 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18353869_1.fastq.gz	Fastqsanger.gz
	SRR18353869_2.fastq.gz	Fastqsanger.gz
	SRR18353870_1.fastq.gz	Fastqsanger.gz
	SRR18353870_2.fastq.gz	Fastqsanger.gz
	SRR18353871_1.fastq.gz	Fastqsanger.gz

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RNA-seq: Transcriptome profile between wild type control and Alk-YS mutant in the Drosophila larval CNS.

Project description:We assessed the differential expression of genes in the Drosophila larval CNS for the Alk mutant and control to understand how the transcriptional responce in Alk-YS mutant.

2022-05-31 | GSE198812 | GEO

The Alk receptor tyrosine kinase regulates Sparkly, a novel activity regulating neuropeptide precursor in the Drosophila CNS

Project description:Numerous roles for the Alk receptor tyrosine kinase have been described in Drosophila, including functions in the CNS, however the molecular details are poorly understood. To gain mechanistic insight, we employed Targeted DamID (TaDa) transcriptional profiling to identify targets of Alk signaling in the larval CNS. TaDa was employed in larval CNS tissues, while genetically manipulating Alk signaling output. The resulting TaDa data were analysed together with larval CNS scRNA-seq datasets performed under similar conditions, identifying a role for Alk in the transcriptional regulation of neuroendocrine gene expression. Further integration with bulk/scRNA-seq and protein datasets from larval brains in which Alk signaling was manipulated, identified a previously uncharacterized Drosophila neuropeptide precursor encoded by CG4577 as an Alk signaling transcriptional target. CG4577, which we named Sparkly (Spar), is expressed in a subset of Alk-positive neuroendocrine cells in the developing larval CNS, including circadian clock neurons. In agreement with our TaDa analysis, overexpression of the Drosophila Alk ligand Jeb resulted in increased levels of Spar protein in the larval CNS. We show that Spar protein is expressed in circadian (Clock) neurons, and Spar mutants exhibit defects in sleep and circadian rhythm control. In summary, we report a novel activity regulating neuropeptide precursor gene that is regulated by Alk signaling in the Drosophila CNS.

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2023-12-01 | E-MTAB-13490 | biostudies-arrayexpress

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Hes mediated transcriptomics in Drosophila larval CNS

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Acetivibrio thermocellus YS strain:YS

Project description:Acetivibrio thermocellus YS strain:YS Genome sequencing

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Acetivibrio thermocellus YS strain:YS

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Olleya sp. YS strain:YS

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Drosophila CNS glial microarray

Project description:Gliogenesis in the Drosophila CNS occurs during embryogenesis and also during the postembryonic larval stages. Several glial subtypes are generated in the postembryonic CNS through the proliferation of differentiated glial cells. The genes and molecular pathways that regulate glial proliferation in the postembryonic CNS are poorly understood. In this study we aimed to use gene expressing profiling of CNS tissue enriched in glia to identify genes expressed in glial cells in the postembryonic CNS. We used microarrays to compare the gene expression profiles from the larval CNS of animals that had increased numbers of glial cells to identify genes that are expressed in glia. RNA was purified from the late third instar larval CNS from control larvae, or larvae expressing an activated form of the FGF receptor (Hlt[ACT]), or overexpressing the insulin receptor (InR) in glial cells using the glial specific driver repoGal4 to increase the number of glial cells and generate CNS tissue enriched in glia.

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Neuroblastoma-associated mutations in Drosophila Alk peturb neuronal differentiation and promote neuronal survival.

Project description:Activating mutations in the Anaplastic Lymphoma Kinase (ALK) receptor tyrosine kinase (RTK) are found in pediatric neuroblastoma, where they are often associated with poor prognosis. To study the effects of ALK-activating mutations in a genetically controllable system we employed CRIPSR/Cas9 to incorporate orthologues of the oncogenic human driver mutations ALKF1174 and ALKY1278S in the Drosophila Alk locus. AlkF1251 and AlkY1355S mutant Drosophila exhibit phenotypes similar to that previously associated with enhanced Alk signaling. Unexpectedly, both mutant alleles are still dependent on the presence of Jeb ligand for activation, as neither can rescue mutants of the Alk ligand Jeb. However, both Alk mutant third instar brains display hyperplasia, represented by increased numbers of Alk-positive neuronal populations. Despite this hyperplasic phenotype within the central brain area, no brain tumors were observed in mutant animals. Further investigation indicated that larval brain hyperplasia in Alk mutants was not caused by significantly increased rates of proliferation, but rather by decreased levels of apoptosis in the larval brain. Using single cell RNA sequencing (scRNAseq) analysis, we identify maintained neuronal fate change during the temporal fate specification of in the mushroom body lineages, with AlkY1355S mutants displaying precocious a’b’ neuron identity. These findings shed important light on the role of Alk in perturbation of neurodevelopmental processes and highlight the potential of activating Alk mutations to promote survival in neuronal lineages

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