1. Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda Maryland 20892, USA
2. These authors contributed equally to this work.
3. Present address: Department of Biology, University of Pennsylvania, Pennsylvania 19104,USA.

Correspondence to: David Sturgill^1,2Brian Oliver¹ Correspondence and requests for materials should be addressed to D.S. (Email: davidsturgill@niddk.nih.gov) and B.O. (Email: oliver@helix.nih.gov).

X chromosomes evolve differently from autosomes, but general governing principles have not emerged¹. For example, genes with male-biased expression are under-represented on the X chromosome of D. melanogaster ², but are randomly distributed in the genome of Anopheles gambiae ³. In direct global profiling experiments using species-specific microarrays, we find a nearly identical paucity of genes with male-biased expression on D. melanogaster, D. simulans, D. yakuba, D. ananassae, D. virilis and D. mojavensis X chromosomes. We observe the same under-representation on the neo-X of D. pseudoobscura. It has been suggested that precocious meiotic silencing of the X chromosome accounts for reduced X chromosome male-biased expression in nematodes⁴, mammals⁵ and Drosophila ⁶. We show that X chromosome genes with male-biased expression are under-represented in somatic cells and in mitotic male germ cells. These data are incompatible with simple X chromosome inactivation models. Using expression profiling and comparative sequence analysis, we show that selective gene extinction on the X chromosome, creation of new genes on autosomes and changed genomic location of existing genes contribute to the unusual X chromosome gene content.

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