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Comparative genomic hybridization of human induced pluripotent stem cell lines.

ABSTRACT: The Purpose of this series of experiments is to identify copy number variations, duplications, and deletions in human induced pluripotent stem (hiPSC) cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26786 | GEO | 2011/05/12

SECONDARY ACCESSION(S): PRJNA136259

REPOSITORIES: GEO

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Comparative genomic hybridization of hiPSC stem cell lines.

Project description:The Purpose of this series of experiments is to identify copy number variations, duplications, and deletions in human induced pluripotent stem (hiPSC) cell lines.

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Comparative genomic hybridization of hiPSC stem cell lines.

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Project description:The Purpose of this series of experiments is to identify copy number variations, duplications, and deletions in human embryonic stem (hES) cell lines deposited to the National Stem Cell bank and reveal the difference between different hES cell lines. CGH can achieve these aims at higher resolution. Keywords: comparative genomic hybridization

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Project description:Background: Amyotrophic lateral sclerosis (ALS) is a devastating disorder of the central nervous system that leads to progressive loss of upper and lower motor neurons. Most cases are sporadic and of unknown aetiology. In this study, we screened 71 patients with sporadic ALS for the presence of DNA copy number variations, in order to identify novel candidate disease genes. Methods: We have used sub-megabase resolution BAC array comparative genomic hybridisation to detect genomic imbalances in our ALS patient cohort. In order to distinguish phenotypically neutral copy number variations occurring frequently in the normal population from disease-associated aberrations, we screened our results against both the Database of Genomic Variants and a reference data set of approximately 700 normal individuals and probands with other disorders analysed in our laboratory. Aberrations with potential relevance for disease aetiology were verified by oligo array CGH. Findings: In 71 patients with sporadic ALS, we identified a total of six duplications and seven deletions that scored above our threshold. Twelve of these thirteen variations were smaller than 1Mb. Seven were observed exclusively in ALS patients and thus likely play causal roles in the disorder. Analysis of these regions highlighted, for example, the SLC1A7 (EAAT5) glutamate transporter and the kinesin family member KIF9 as good positional and functional candidate genes for ALS. Interpretation: Non-polymorphic sub-microscopic duplications and deletions observable by array CGH are frequent in patients with sporadic ALS. Analysis of such aberrations serves as an excellent starting point in deciphering the aetiology of this complex disease. Keywords: array CGH

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