Selection shapes genome evolution at the DNA sequence level, mainly manifested in changes in the primary structure of genes and other functional elements. A long-standing question in evolutionary biology is whether the organization of genes, their location in different regions of the genome, is also subject to selection (Hurst et al. 2004). A candidate case would be the genomic organization of sexually antagonistic genes, i.e., genes beneficial to one sex but either detrimental or neutral to the other (Rice 1992; Rice and Chippindale 2001; van Doorn 2009). Theoretical arguments imply that such genes are only expected to occur if the benefits accrued to one sex outweigh the disadvantages imposed to the other. However, there is an important exception to this prediction that relates to the special mode of inheritance and organization of sex chromosomes, and to cost-benefit scenarios associated with sex-linkage. For example, as far as partially or fully dominant mutations are considered, theory predicts that it should be easier for an antagonistic gene favorable to one sex to evolve on a sex chromosome that is more often present in that sex than in the other, since net selection will then be positive (Rice 1984; Charlesworth et al. 1987). This leads to the expectation that female-beneficial genes should be over-represented, and male-beneficial genes under-represented, on the X-chromosome in male-heterogametic organisms. In practice, it is difficult on a large scale to determine whether genes are or have been sexually antagonistic. Several investigators have therefore used sex-biased gene expression as a proxy for sexual antagonism (see Ellegren and Parsch 2007); sex-biased gene expression may potentially represent the resolution of past sexual antagonism (e.g., Mank and Ellegren 2009). This line of thinking has been integrated with several observations of a non-random genomic distribution of genes with sex-biased expression. In Drosophila, male-biased genes are under-represented on the X (Parisi et al. 2003; Sturgill et al. 2007; Vicoso and Charlesworth 2009). If this is translated into an under-representation of male-beneficial genes on X, it would be consistent with theory for partly or fully dominant mutations (Rice 1984). In Caenorhabditis elegans, sperm-enriched genes are nearly absent from the X-chromosome (Reinke et al. 2000). In mammals, the picture is more complex. Female-biased genes expressed in ovary and placenta are over-represented on the mouse X-chromosome (Khil et al. 2004), also as expected for dominant mutations. However, male-biased genes expressed in early stages of spermatogenesis are in excess on the mouse X as well (Khil et al. 2004), although genes expressed later during male meiosis are, in fact, under-represented on the X (Khil et al. 2004). Several alternative explanations to the non-random distribution of sex-biased genes have therefore been suggested (Rogers et al. 2003; Meisel et al. 2009), including escape from meiotic sex chromosome inactivation (MSCI) by genes needed to be expressed during spermatogenesis (Hense et al. 2007; Potrzebowski et al. 2008; Vibranovski et al. 2009a). A limitation in the abovementioned empirical studies is that they survey the overall present-day gene content of different chromosomal categories rather than specifically focusing on the characteristics of those new genes that evolved in different regions of the genome (cf. Zhang et al. 2010). However, the arguments for the probability of evolution of sexually antagonistic alleles in different chromosomal categories can also be applied to different scenarios of movement of genes between sex chromosomes and autosomes (Moyle et al. 2010). Relevant in this context are empirical data on traffic of retrogenes between autosomes and the X-chromosome in mammals and Drosophila (Betran et al. 2002; Emerson et al. 2004; Vibranovski et al. 2009b), in particular, a pattern that has been referred to as “out-of-X movement.” It has been noted that many retrotransposed gene copies moving from the X-chromosome to autosomes have acquired sex-biased gene expression and are mainly expressed in testis (Bradley et al. 2004). In the seminal study by Emerson et al. (2004), it was hypothesized that natural selection has favored the preservation of genes with male-biased function that move from the X-chromosome to autosomes: “One model of sexual antagonism (Wu and Yujun Xu 2003) predicts that gene copies that benefit males at a cost to females would be more likely found on the autosomes than on the X-chromosome.” Note again that sex-biased gene expression is taken as a proxy for sexual antagonism. A potentially interesting contrast in testing an adaptive scenario for the genomic distribution of new sex-biased genes is to study organisms with female heterogamety (males ZZ, females ZW). In this case, male-beneficial genes in which new mutations are at least partly dominant may be expected to accumulate on the Z-chromosome, rather than on autosomes, because Z is two-thirds of the time in males. With the same argument, female-beneficial genes would be expected to become less abundant on the Z-chromosome. These opposing predictions compared to systems of male heterogamety are helpful for the general argument because they allow distinguishing the expected effects of heterogamety from any other difference that pertain to autosomes and sex chromosomes. Female heterogamety is found in a diverse range of organisms. All birds are female heterogametic, and the same applies to all butterflies. A ZW sex chromosome system is also present in individual lineages of reptiles, amphibians, fishes, and crustaceans. Although draft genome sequences of a few female heterogametic bird species (chicken, Gallus gallus [International Chicken Genome Sequencing Consortium 2004]; zebra finch, Taeniopygia guttata [Warren et al. 2010]; and turkey [Dalloul et al. 2010]) and one moth (silkworm, Bombyx mori [Mita et al. 2004; Xia et al. 2004]) have been reported, the coverage of the Z-chromosome has generally not been sufficient for a comprehensive analysis of gene content. However, the recent sequencing to near completion of the chicken Z-chromosome (Bellott et al. 2010) provides a framework for a test of the emergence of new genes on sex chromosomes in a female heterogametic system. The chicken Z-chromosome is 80 Mb in size and contains about 1000 genes. The female-specific W-chromosome is less well characterized, but it is considerably smaller, mostly non-recombining, and contains a limited number of paralogs (gametologs) to Z-linked genes as well as some female-specific genes (Ellegren 2000; International Chicken Genome Sequencing Consortium 2004). The avian ZW and the mammalian XY sex chromosomes evolved independently from different pairs of autosomes present in a vertebrate ancestor (Fridolfsson et al. 1998; Nanda et al. 1999; Bellott et al. 2010). They thereby offer parallel biological replicates to the study of sex chromosome evolution and the associated question of genome organization potentially driven by selectively favorable gene acquisitions.