Ontology highlight
ABSTRACT:
PROVIDER: PRJNA369717 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5226820.fastq.gz | Fastqsanger.gz | |||
| SRR5226830.fastq.gz | Fastqsanger.gz | |||
| SRR5226840.fastq.gz | Fastqsanger.gz | |||
| SRR5226840_1.fastq.gz | Fastqsanger.gz | |||
| SRR5226840_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 190 |
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Project description:Indicated cells were subjected to RNAi against linker histone H1, Nautilus (control), or GFP (control). RNA was isolated and subjected to Affymetrix GeneChIP Drosophila Genome 2.0 arrays RNA was compared from cells treated with RNAi against control (Nautilus in the case of salivary glands or GFP in the case of Kc cells) and linker histone H1. Kc cells were treated once with RNAi and RNA was collected 6 days later.
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Project description:Loss of nautilus (MyoD) gene function results in a variable phenotype affecting muscle formation in embryos and larvae, larval movement, pupal eclosion, egg deposition, adult mobility and survival. 8-miR cluster deletion disrupts muscle formation in the embryo while affecting protein production from the nautilus, dMef2 , regulators of the muscle transcriptional network. We propose the complex phenotype in the nautilus null is due to the disruption of the regulatory interactions provided by the 8-miR cluster. The results demonstrate that nautilus is an integral regulator of the miRNA circuitry buffering the transcriptional network directing muscle development.
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Project description:To determine if the Drosophila MyoD homolog, nautilus, was activating any miRNA loci, similar to vertebrate MyoD, we compared the miRNA expression profiles between wild-type (w1118) and nautilus null embryos during the window of maximum nautilus expression (6-8hr AEL), using LNA arrays specifically designed to quantify miRNA levels in Drosophila (Exiqon). Expression levels for mir-309, mir-3, mir-286, mir-4, mir-5, and mir-6 from the 8-miR cluster, were significantly decreased in nautilus null embryos. It suggests that the intergenic 8-miR cluster, encoding eight miRNAs, is regulated by nautilus. Two-condition experiment, wild type (w1118) vs. mutant (nautilus null). Biological replicates: 3 wild type, 3 mutants, independently isolated.
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Project description:Salivary glands or larval ovaries were isolated from transgenic flies expressing RNAi targeting Nautilus (control) or linker histone H1 using a Tub-Gal4 driver.
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Project description:Loss of nautilus (MyoD) gene function results in a variable phenotype affecting muscle formation in embryos and larvae, larval movement, pupal eclosion, egg deposition, adult mobility and survival. mir-3 over expression disrupts muscle formation in the embryo while affecting protein production from the dMef2 and tinman genes, global regulators of the muscle transcriptional network. We propose the complex phenotype in the nautilus null is due to the disruption of the regulatory interactions provided by the 8-miR cluster. The results demonstrate that nautilus is an integral regulator of the miRNA circuitry buffering the transcriptional network directing muscle development.
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