Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from cochlea isolated from N-myc mutant and wild-type mice at E15

ABSTRACT: The aim of this study consists in detecting genes regulated by N-myc in the murine cochlea In this data set we present 2688 genes differentially regulated by Nmyc in the murine cochlea. These data serve as a platform for verifying their differential regulation by N-myc via RNA in situ hybridisation or other techniques. 4 Total samples were analyzed. A pairwise comparison between two wild-type and 2 N-myc mutants samples was conducted. Genes with a FDR up to 14% are presented. Briefly, the robust microarray analysis (RMA) algorithm was used for background correction, intra- and inter-microarray normalization, and expression signal calculation. Once the absolute expression signal for each gene (i.e., the signal value for each probe set) was calculated in each microarray, a method [called significance analysis of microarray (SAM)] was applied to calculate significant differential expression and find the gene probe sets that characterized the highly metastatic samples. The method uses permutations to provide robust statistical inference of the most significant genes and provides P valuesadjusted to multiple testing using false discovery rate (FDR).

ORGANISM(S): Mus musculus

SUBMITTER: Thomas Schimmang

PROVIDER: E-GEOD-61406 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Spiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves. Analysis was conducted on auditory nerve samples from stages encompassing maturation and onset of hearing. Cochleas were collected from euthanized mice (CBA/CaJ) at perinatal (P) stages P0, P3, P7, P10, P14 and P21. Cochleas underwent microdissection to remove the outer bony cochlear shell and cochlear lateral wall, thus preserving the modiolus portion of cochlea which contains mainly the auditory nerve. Paired cochleas (i.e., from left and right ears) from each mouse were pooled to make individual samples. All sample types were done in experimental duplicate (n=2).

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Expression data from cochlea isolated from N-myc mutant and wild-type mice at E15

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