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Array CGH with DNA extracted from Candida albicans strains and its derivatives, which is monosomic for chromosome 5

ABSTRACT: Goal of this experiment was to confirm the proposed monosomy condition of chromsome 5 genes in the derivatives

ORGANISM(S): Candida albicans

PROVIDER: GSE48093 | GEO | 2013/11/04

SECONDARY ACCESSION(S): PRJNA208920

REPOSITORIES: GEO

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Array CGH with DNA extracted from Candida albicans strains and its derivatives, which is monosomic for chromosome 5

Project description:Goal of this experiment was to confirm the proposed monosomy condition of chromsome 5 genes in the derivatives Pair-wise comparison of genomic content between parental strains and their derivatives.

2013-11-04 | E-GEOD-48093 | biostudies-arrayexpress

Array CGH with DNA extracted from Candida albicans strains 3153A and its derivative Sor55, which is monosomic for chromosome 5

Project description:Goal of this experiment was to confirm the proposed monosomy condition of chromsome 5 genes in the mutant Sor55

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Array CGH with DNA extracted from Candida albicans strains 3153A and its derivative Sor55, which is monosomic for chromosome 5

Project description:Goal of this experiment was to confirm the proposed monosomy condition of chromsome 5 genes in the mutant Sor55 Different batches of total DNA were prepared from the parental strain 3153A and its derivative Sor55. Hybridization included different combinations of two independent batches of DNA from 3153A or Sor55, as well as one dye-swap. Parental/mutant ratio data was analyzed.

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Monosomic chr5 derivative of laboratory strain of Candida albicans 3153A

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Proteomic analysis of human monosomic cell lines

Project description:Chromosome loss that results in monosomy has detrimental consequences for human cells, but the underlying molecular mechanisms remain enigmatic. Using p53 deficient monosomic cell lines, we found that chromosome loss impairs proliferation and genomic stability. Transcriptome and proteome analysis revealed a partial compensation of the gene dosage changes that mitigates the effects of chromosome loss. Monosomy triggers global gene expression changes that differ from the effects of trisomy. Strikingly, ribosome biogenesis and translation were commonly downregulated in monosomic cells. Polysome profiling and translation analysis suggest that the defects arise due to haploinsufficiency of ribosomal genes. The ensuing ribosome biogenesis stress triggers the p53 pathway and G1 arrest when TP53 is reintroduced into monosomic cells. Accordingly, impaired ribosome biogenesis and p53 inactivation are associated with monosomy in cancer. Our first systematic study of monosomy in human cells demonstrates that haploinsufficiency of ribosomal genes presents a dominant negative phenotype of monosomy.

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