Abundance of female-biased and paucity of male-biased somatically expressed genes on the mouse X-chromosome
1 Department of Organismal Biology, Evolutionary Biology Centre, Uppsala University, Uppsala, Sweden
2 Ludwig Institute for Cancer Research, Stockholm, Sweden
3 Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden
4 School of Life Sciences, University of Sussex, Brighton, United Kingdom
5 Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden
6 Department of Medical and Clinical Genetics, Department of Biomedicine, The Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden
7 Department of Anatomy and Neurobiology, University of Tennessee, Knoxville, USA
Citation and License
BMC Genomics 2012, 13:607 doi:10.1186/1471-2164-13-607Published: 10 November 2012
Empirical evaluations of sexually dimorphic expression of genes on the mammalian X-chromosome are needed to understand the evolutionary forces and the gene-regulatory mechanisms controlling this chromosome. We performed a large-scale sex-bias expression analysis of genes on the X-chromosome in six different somatic tissues from mouse.
Our results show that the mouse X-chromosome is enriched with female-biased genes and depleted of male-biased genes. This suggests that feminisation as well as de-masculinisation of the X-chromosome has occurred in terms of gene expression in non-reproductive tissues. Several mechanisms may be responsible for the control of female-biased expression on chromosome X, and escape from X-inactivation is a main candidate. We confirmed escape in case of Tmem29 using RNA-FISH analysis. In addition, we identified novel female-biased non-coding transcripts located in the same female-biased cluster as the well-known coding X-inactivation escapee Kdm5c, likely transcribed from the transition-region between active and silenced domains. We also found that previously known escapees only partially explained the overrepresentation of female-biased X-genes, particularly for tissue-specific female-biased genes. Therefore, the gene set we have identified contains tissue-specific escapees and/or genes controlled by other sexually skewed regulatory mechanisms. Analysis of gene age showed that evolutionarily old X-genes (>100 myr, preceding the radiation of placental mammals) are more frequently female-biased than younger genes.
Altogether, our results have implications for understanding both gene regulation and gene evolution of mammalian X-chromosomes, and suggest that the final result in terms of the X-gene composition (masculinisation versus feminisation) is a compromise between different evolutionary forces acting on reproductive and somatic tissues.