Transcriptomics

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Expression data from Gdap1 knock-out (deletion of exon 5) mice


ABSTRACT: GDAP1 is a mitochondrial fission factor and mutations in GDAP1 cause Charcot-Marie-Tooth disease. Gdap1 knockout mice, mimicking genetic alterations of patients suffering from severe CMT forms, develop an age-related, hypomyelinating peripheral neuropathy. We used microarrays to determine changes in the expression profiles in the peripheral nervous system before a phenotype was detectable in the animal model (2 month of age). To seek changes in gene expression patterns of Gdap1-/- mice, we isolated motoneurons by laser dissection and took sciatic nerve lysates of two-month-old mice and purified RNA of five mice. Based on the amount and quality of the isolated RNA we selected three samples per tissue (sciatic nerve lysate and motoneruons) and genotype (GDAP1-/- or wild type). Note: the probe sets for Gdap1 lie within exon 4 and exon 6, thus no apparent loss of Gdap1 mRNA expression is present in Gdap1-/- animals.

REANALYSED by: E-GEOD-51650

ORGANISM(S): Mus musculus  

SUBMITTER: U Suter   A Niemann  H Halfter  Axel Niemann  P Young 

PROVIDER: E-GEOD-51650 | ArrayExpress | 2014-01-03

SECONDARY ACCESSION(S): GSE51650PRJNA224198

REPOSITORIES: GEO, ArrayExpress

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Publications


The ganglioside-induced differentiation-associated protein 1 (GDAP1) is a mitochondrial fission factor and mutations in GDAP1 cause Charcot-Marie-Tooth disease. We found that Gdap1 knockout mice (Gdap1(-/-)), mimicking genetic alterations of patients suffering from severe forms of Charcot-Marie-Tooth disease, develop an age-related, hypomyelinating peripheral neuropathy. Ablation of Gdap1 expression in Schwann cells recapitulates this phenotype. Additionally, intra-axonal mitochondria of periphe  ...[more]

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