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Expression data from human triploid and diploid fibroblast cell cultures


ABSTRACT: Dosage compensation restores a balanced network of gene expression between autosomes and sex chromosomes in males (XY) and females (XX). In mammals, this is achieved by doubling the expression of X-linked genes in both sexes, together with X inactivation in females. X up-regulation may be controlled by DNA sequence based and/or epigenetic mechanisms that double the X output potentially in response to an autosomal counting factor. Human triploids with either one or two active X chromosomes (Xa) provide a mean to test X chromosome expression in the presence of three sets of autosomes, which will help understand the underlying mechanisms of X up-regulation. We measured whole genome gene expression in human triploid cell cultures with either one or two active X. We found that overall X-linked gene expression is not tripled in the presence of three sets of autosomes. However, in triploid cells with a single active X chromosome, its expression is adjusted upward, presumably by an epigenetic mechanism that senses the active X-autosome ratio. Six human XXX triploid fibroblast clones with either one or two active X, three XYY triploid fibroblast cultures, and two male (XY) and two female (XaXi) control diploid fibroblast cultures were selected for RNA extraction and hybridization on Affymetrix whole genome expression arrays (HG-U133 2.0 plus chip). Probe labeling, array hybridization and scanning were done by the University of Washington Microarray Center.

ORGANISM(S): Homo sapiens

SUBMITTER: Xinxian Deng 

PROVIDER: E-GEOD-18877 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Dosage regulation of the active X chromosome in human triploid cells.

Deng Xinxian X   Nguyen Di Kim DK   Hansen R Scott RS   Van Dyke Daniel L DL   Gartler Stanley M SM   Disteche Christine M CM  

PLoS genetics 20091204 12


In mammals, dosage compensation is achieved by doubling expression of X-linked genes in both sexes, together with X inactivation in females. Up-regulation of the active X chromosome may be controlled by DNA sequence-based and/or epigenetic mechanisms that double the X output potentially in response to autosomal factor(s). To determine whether X expression is adjusted depending on ploidy, we used expression arrays to compare X-linked and autosomal gene expression in human triploid cells. While th  ...[more]

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