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Gene expression profile of supernumerary type II neuroblasts transiently overexpressing Insb

ABSTRACT: Gene expression profile of supernumerary type II neuroblasts transiently overexpressing Insb

PROVIDER: PRJNA639873 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12030903.fastq.gz	Fastqsanger.gz
	SRR12030904.fastq.gz	Fastqsanger.gz
	SRR12030905.fastq.gz	Fastqsanger.gz
	SRR12030906.fastq.gz	Fastqsanger.gz
	SRR12030907.fastq.gz	Fastqsanger.gz

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Gene expression profile of supernumerary type II neuroblasts transiently overexpressing Insb

Project description:Genes that positively regulate neuroblast functional identity shoud be expressed in type II neuroblasts and become repidly downregulated in immature INPs in wild-type brains while genes that suppress neuroblast functional idnetity should be upregulated in immature INPs. The goal of this study is to identify genes involved in regulation of type II neuroblast functional identity.

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Project description:A brain consists of numerous distinct neurons arising from a limited number of progenitors, called neuroblasts in Drosophila. Each neuroblast makes a specific neuronal lineage. To unravel the transcriptional networks that underlie the development of distinct neuroblast lineages, we marked and isolated lineage-specific neuroblasts for RNA sequencing. We labeled particular neuroblasts throughout neurogenesis by activating a conditional neuroblast driver in specific lineages using various intersection strategies. The targeted neuroblasts were efficiently recovered using a custom-built device for robotic single cell picking. Transcriptome analysis on the mushroom body, antennal lobe, and type II neuroblasts besides non-selective neuroblasts, neurons, and glia revealed a rich repertoire of transcription factors expressed among neuroblasts in diverse patterns. In addition to those likely pan-neuroblast transcription factors, there exist many transcription factors selectively enriched or repressed in certain neuroblasts. The unique combinations of transcription factors present in different neuroblasts may govern the diverse lineage-specific neuron fates

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Transcription profiling of GR-N-91 neuroblasts injected subcutaneously into nude mice and a primary tumor Xenograft (PTX) was isolated whilst metastatic neuroblasts were isolated from Myocardium (MY) and Bone Marrow (BM)

Project description:We have used an IGR-N-91 parental cell line established from an involved bone marrow harvested from a high-risk NB (stage 4-NB, 8 year-old boy). These IGR-N-91 neuroblasts were injected subcutaneously into nude mice and a Primary Tumor Xenograft (PTX) was isolated whilst metastatic neuroblasts were isolated from Myocardium (MY) and Bone Marrow (BM). These malignant neuroblasts were further cultured in vitro on bovine corneal extra-cellular matrix to establish sublines (IGR/PTX, IGR/BM and IGR/MY). Agilent oligo microarray analysis was performed to compare gene expression profiles in BM and MY metastatic versus PTX neuroblasts. This analysis used eight microarrays (two replicates plus two dye-swap experiments for both MY and BM cell lines).

2006-09-11 | E-TABM-44 | biostudies-arrayexpress

Homeodomain protein Six4 prevents the generation of supernumerary Drosophila type II neuroblasts and premature differentiation of intermediate neural progenitors.

Project description:In order to boost the number and diversity of neurons generated from neural stem cells, intermediate neural progenitors (INPs) need to maintain their homeostasis by avoiding both dedifferentiation and premature differentiation. Elucidating how INPs maintain homeostasis is critical for understanding the generation of brain complexity and various neurological diseases resulting from defects in INP development. Here we report that Six4 expressed in Drosophila type II neuroblast (NB) lineages prevents the generation of supernumerary type II NBs and premature differentiation of INPs. We show that loss of Six4 leads to supernumerary type II NBs likely due to dedifferentiation of immature INPs (imINPs). We provide data to further demonstrate that Six4 inhibits the expression and activity of PntP1 in imINPs in part by forming a trimeric complex with Earmuff and PntP1. Furthermore, knockdown of Six4 exacerbates the loss of INPs resulting from the loss of PntP1 by enhancing ectopic Prospero expression in imINPs, suggesting that Six4 is also required for preventing premature differentiation of INPs. Taken together, our work identified a novel transcription factor that likely plays important roles in maintaining INP homeostasis.

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