BACKGROUND: X monosomic mice (39,XO) have a remarkably mild phenotype when 
compared to women with Turner syndrome (45,XO). The generally accepted 
hypothesis to explain this discrepancy is that the number of genes on the mouse 
X chromosome which escape X inactivation, and thus are expressed at higher 
levels in females, is very small. However this hypothesis has never been tested 
and only a small number of genes have been assayed for their X-inactivation 
status in the mouse. We performed a global expression analysis in four somatic 
tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice using 
the Illumina Mouse WG-6 v1_1 Expression BeadChip and an extensive validation by 
quantitative real time PCR, in order to identify which genes are expressed from 
both X chromosomes.
RESULTS: We identified several genes on the X chromosome which are overexpressed 
in XX females, including those previously reported as escaping X inactivation, 
as well as new candidates. However, the results obtained by microarray and qPCR 
were not fully concordant, illustrating the difficulty in ascertaining modest 
fold changes, such as those expected for genes escaping X inactivation. 
Remarkably, considerable variation was observed between tissues, suggesting that 
inactivation patterns may be tissue-dependent. Our analysis also exposed several 
autosomal genes involved in mitochondrial metabolism and in protein translation 
which are differentially expressed between XX and XO mice, revealing secondary 
transcriptional changes to the alteration in X chromosome dosage.
CONCLUSIONS: Our results support the prediction that the mouse inactive X 
chromosome is largely silent, while providing a list of the genes potentially 
escaping X inactivation in rodents. Although the lower expression of X-linked 
genes in XO mice may not be relevant in the particular tissues/systems which are 
affected in human X chromosome monosomy, genes deregulated in XO mice are good 
candidates for further study in an involvement in Turner Syndrome phenotype.