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RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96

ABSTRACT: RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96

PROVIDER: PRJEB21214 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2002990_1.fastq.gz	Fastqsanger.gz
	ERR2002990_2.fastq.gz	Fastqsanger.gz
	ERR2003000_1.fastq.gz	Fastqsanger.gz
	ERR2003000_2.fastq.gz	Fastqsanger.gz
	ERR2003010_1.fastq.gz	Fastqsanger.gz

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RNA-seq of organ of Corti RNA from mice carrying a null allele of Mir183 and Mir96

Project description:The microRNA miR-96 is important for hearing; mutations in the seed region result in dominant progressive hearing loss in mice and humans. Mir96 is expressed in the sensory hair cells of the organ of Corti along with Mir182 and Mir183. miR-96 is a master regulator of hair cell development, controlling many genes in the organ of Corti, but the role of miR-182 and miR-183 in the hair cells is unknown. We carried out RNA-seq on mice carrying a knockout allele of Mir182, and mice carrying a double knockout allele of Mir183 and Mir96 (Mir183/96). RNA was extracted from the organ of Corti from P4 homozygotes and sex-matched wildtype littermates. Strand-specific libraries were prepared using the NuGEN Ovation Mouse RNA-Seq System 1-16 kit and sequenced on an Illumina HiSeq 2500 machine as paired-end 125bp reads.

2019-03-15 | E-MTAB-5800 | biostudies-arrayexpress

RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

Project description:Mutations affecting the microRNA miR-96 have been found to cause progressive hearing loss in humans and in mice. These initial mutations were all semidominant, so phenotypes were present in heterozygous carriers. The similarity of the phenotype between the different mutations suggested that it was the loss of normal function of Mir96 that underlay the hearing impairment. However, more recent studies of null alleles of Mir96 and the nearby Mir183, and of Mir96, Mir182 and Mir183 all together, showed that heterozygous carriers of the null alleles have no hearing phenotype, suggesting that the gain of novel targets due to the changed seed sequence resulting from point mutations is important in the Mir96 mutant phenotype, not just the loss of normal targeting. Previous transcriptome analyses of the Mir96 mutant organ of Corti showed that miR-96 controls a broad regulatory network, suggesting that a better understanding of the core genes – particularly the direct targets of miR-96 – may suggest candidate therapeutic targets. We carried out RNA-seq on mice carrying the two seed region point mutations reported in human families. RNA was extracted from the organ of Corti from four day-old homozygotes and sex-matched wildtype littermates. Strand-specific libraries were prepared following the “TruSeq Stranded mRNA Sample Preparation Guide” with the corresponding kit [Illumina Inc. Cat.# RS-122-2101 or RS-122-2102], and sequenced on an Illumina HiSeq 4000 machine as paired-end 101bp reads.

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RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

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Project description:RNAseq of organ of Corti RNA from mice carrying human mutations in Mir96

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