Dosage compensation balances gene expression levels between the sex chromosomes and autosomes and sex-chromosome-linked gene expression levels between the sexes. Different dosage compensation strategies evolved in different lineages, but all involve changes in chromatin. This paper discusses our current understanding of how modifications of the histone H4 tail, particularly changes in levels of H4 lysine 16 acetylation and H4 lysine 20 methylation, can be used in different contexts to either modulate gene expression levels twofold or to completely inhibit transcription. 1. Need for Dosage Compensation Proper chromosome dosage is essential for the viability and fitness of an organism [1]. Most variations in chromosome quantity (aneuploidies) are inviable [1]. Some aneuploidies are tolerated, but result in severe developmental phenotypes, including Down syndrome, trisomy 21 [1]. However, a difference in sex chromosome copy number must be accommodated across many species. Sex can be determined by sex chromosomes, where one sex is homogametic for the sex chromosome, while the other is heterogametic. In the XY sex chromosome system, females have two X chromosomes, and males are XY or XO. In the ZW system, males are ZZ, and females are ZW. As a consequence of these differences, the heterogametic sex is functionally monosomic for the sex chromosome. The X and Z chromosomes encode genes involved in many processes required for life, not just sex-specific processes. To cope with this disparity, dosage compensation balances the expression of the sex chromosomes to the diploid autosomes and equalizes sex chromosome expression between males and females. Dosage compensation has been studied in mammals, worms, flies, and birds. These organisms all cope with sex chromosome imbalance between males and females; however the mechanisms and machineries that they use differ widely (Figure 1). In the fly Drosophila melanogaster, XY males upregulate their single X chromosome twofold [2]. This process accomplishes both goals: it balances expression of the single X with autosomes and also equalizes X-linked gene dosage in the sexes. Although less well understood mechanistically, X chromosome upregulation is thought to occur in both sexes in mammals [3, 4]. While this balances the genome in XY males, it causes overexpression of the X chromosomes in XX females. A second (and better understood) mechanism then inactivates one of the two X chromosomes in females, thereby equalizing X expression [5]. In the nematode C. elegans, the X chromosomes are thought to be upregulated in both
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