Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Review Article
  • Published:

Dosage compensation: the beginning and end of generalization

Nature Reviews Genetics volume 8, pages 47–57 (2007)Cite this article

Key Points

  • Unbalanced gene expression that is due to unequal distribution of sex chromosomes in mammals, worms and flies is counteracted by specific compensation processes. Recent research has shown that upregulation of transcription from the single male X chromosome might be common to all systems.

  • Whereas upregulation of the X chromosome is restricted to males in Drosophila melanogaster, it occurs in both sexes in mammals and worms. Consequently, female mammals and hermaphrodite worms have to counteract enhanced X-chromosome transcription by repressive measures.

  • Dosage compensation processes are chromosome-specific; however, they do not affect all genes to the same extent, with a large number of genes completely escaping the process. Adopting compensation seems to be a gene-specific feature rather than a uniform, chromosome-wide property.

  • The machineries involved in compensation are distinct; however they all alter chromatin structure to modulate gene expression.

  • High-resolution mapping of the dosage compensation complex (DCC) in D. melanogaster revealed preferred binding to transcribed sequences. This feature distinguishes these proteins from classical transcription factors and indicates that increased gene expression is achieved by facilitated transcription elongation.

  • The targeting principles of the DCC in worm and flies are complex as simple DNA recognition motifs could not be identified. In flies, the combination of a multitude of DNA motifs and active transcription might determine chromosome-specific and gene-specific binding.

Abstract

The genomes of higher eukaryotes are carefully balanced systems of gene expression that compensate for the different numbers of sex chromosomes in the two sexes by adjusting gene expression levels. Different strategies for sex chromosome dosage compensation have evolved, which all involve modulating chromatin structure as a means to fine-tune transcription levels. As data accumulate, previous over-simplifications are being revised, and novel features of the compensation processes are gaining attention, many of which are of sufficient global validity to influence our view on gene expression beyond the realm of dosage compensation itself.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Principles of X-chromosome dosage compensation.
Figure 2: Composition of the Drosophila melanogaster DCC.
Figure 3: X-chromosome bloating in ISWI/ISWI males.
Figure 4: The Caenorhabditis elegans DCC.
Figure 5: Chromosome-wide distribution of dosage compensation.
Figure 6: Gain of resolution by a ChIP-on-chip array.
Figure 7: Targeting models for the Drosophila melanogaster DCC.

Similar content being viewed by others

References

  1. Larsson, J. & Meller, V. H. Dosage compensation, the origin and the afterlife of sex chromosomes. Chromosome Res. 14, 417–431 (2006).

    Article  CAS  PubMed  Google Scholar 

  2. Khil, P. P. & Camerini-Otero, R. D. Molecular features and functional constraints in the evolution of the mammalian X chromosome. Crit. Rev. Biochem. Mol. Biol. 40, 313–330 (2005).

    Article  CAS  PubMed  Google Scholar 

  3. Vicoso, B. & Charlesworth, B. Evolution of the X chromosome: unusual patterns and processes. Nature Rev. Genet. 7, 645–653 (2006).

    Article  CAS  PubMed  Google Scholar 

  4. Lucchesi, J. C., Kelly, W. G. & Panning, B. Chromatin remodeling in dosage compensation. Annu. Rev. Genet. 39, 615–651 (2005).

    Article  CAS  PubMed  Google Scholar 

  5. Lucchesi, J. C. Dosage compensation in Drosophila. Annu. Rev. Genet. 7, 225–237 (1973).

    Article  CAS  PubMed  Google Scholar 

  6. Gupta, V. et al. Global analysis of X-chromosome dosage compensation. J. Biol. 5, 3 (2006).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  7. Nguyen, D. K. & Disteche, C. M. Dosage compensation of the active X chromosome in mammals. Nature Genet. 38, 47–53 (2006). References 6 and 7 describe large-scale microarray analyses revealing that, apart from Drosophila melanogaster , upregulation of transcription from the single male X chromosome occurs in Caenorhabditis elegans and mammals.

    Article  CAS  PubMed  Google Scholar 

  8. Hamada, F. N., Park, P. J., Gordadze, P. R. & Kuroda, M. I. Global regulation of X chromosomal genes by the MSL complex in Drosophila melanogaster. Genes Dev. 19, 2289–2294 (2005). This study describes an expression microarray analysis which indicates that the increase in transcription of most of the X-linked genes by the MSL complex is graded rather than strictly twofold.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Straub, T., Gilfillan, G. D., Maier, V. K. & Becker, P. B. The Drosophila MSL complex activates the transcription of target genes. Genes Dev. 19, 2284–2288 (2005). The first study to prove the direct link between MSL binding and increased expression of specific genes.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Alekseyenko, A. A., Larschan, E., Lai, W. R., Park, P. J. & Kuroda, M. I. High-resolution ChIP–chip analysis reveals that the Drosophila MSL complex selectively identifies active genes on the male X chromosome. Genes Dev. 20, 848–857 (2006). A comparative ChIP-on-chip tiling array study of MSL3 binding in D. melanogaster cell lines and embryos favouring a transcription-based model of MSL complex recruitment.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Gilfillan, G. D. et al. Chromosome-wide gene-specific targeting of the Drosophila dosage compensation complex. Genes Dev. 20, 858–870 (2006). MSL1 and RNA Polymerase II profiling using ChIP-on-chip tiling arrays in D. melanogaster embryos. Complex combinations of degenerate sequence motifs can in part explain the MSL binding pattern.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Legube, G., McWeeney, S. K., Lercher, M. J. & Akhtar, A. X-chromosome-wide profiling of MSL-1 distribution and dosage compensation in Drosophila. Genes Dev. 20, 871–883 (2006). A ChiP-on-cDNA array study comparing MSL1 distribution in different developmental stages and tissues of D. melanogaster . The MSL binding pattern is stable and does not correlate with transcription.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Steinemann, M., Steinemann, S. & Turner, B. M. Evolution of dosage compensation. Chromosome Res. 4, 185–190 (1996).

    Article  CAS  PubMed  Google Scholar 

  14. Charlesworth, B. The evolution of chromosomal sex determination and dosage compensation. Curr. Biol. 6, 149–162 (1996).

    Article  CAS  PubMed  Google Scholar 

  15. Lyon, M. F. Gene action in the X-chromosome of the mouse (Mus musculus L.). Nature 190, 372–373 (1961).

    Article  CAS  PubMed  Google Scholar 

  16. Meyer, B. J. & Casson, L. P. Caenorhabditis elegans compensates for the difference in X chromosome dosage between the sexes by regulating transcript levels. Cell 47, 871–881 (1986).

    Article  CAS  PubMed  Google Scholar 

  17. Heard, E. & Disteche, C. M. Dosage compensation in mammals: fine-tuning the expression of the X chromosome. Genes Dev. 20, 1848–1867 (2006).

    Article  CAS  PubMed  Google Scholar 

  18. Chadwick, B. P. & Willard, H. F. Chromatin of the Barr body: histone and non-histone proteins associated with or excluded from the inactive X chromosome. Hum. Mol. Genet. 12, 2167–2178 (2003).

    Article  CAS  PubMed  Google Scholar 

  19. Mak, W. et al. Mitotically stable association of Polycomb group proteins eed and enx1 with the inactive X chromosome in trophoblast stem cells. Curr. Biol. 12, 1016–1020 (2002).

    Article  CAS  PubMed  Google Scholar 

  20. Costanzi, C. & Pehrson, J. R. Histone macroH2A1 is concentrated in the inactive X chromosome of female mammals. Nature 393, 599–601 (1998).

    Article  CAS  PubMed  Google Scholar 

  21. Mohandas, T., Sparkes, R. S. & Shapiro, L. J. Reactivation of an inactive human X chromosome: evidence for X inactivation by DNA methylation. Science 211, 393–396 (1981).

    Article  CAS  PubMed  Google Scholar 

  22. Dorigo, B., Schalch, T., Bystricky, K. & Richmond, T. J. Chromatin fiber folding: requirement for the histone H4 N-terminal tail. J. Mol. Biol. 327, 85–96 (2003).

    Article  CAS  PubMed  Google Scholar 

  23. Shogren-Knaak, M. et al. Histone H4-K16 acetylation controls chromatin structure and protein interactions. Science 311, 844–847 (2006).

    Article  CAS  PubMed  Google Scholar 

  24. Deuring, R. et al. The ISWI chromatin remodeling protein is required for gene expression and the maintenance of higher order chromatin structure in vivo. Mol. Cell 5, 355–365 (2000).

    Article  CAS  PubMed  Google Scholar 

  25. Badenhorst, P., Voas, M., Rebay, I. & Wu, C. Biological functions of the ISWI chromatin remodeling complex NURF. Genes Dev. 16, 3186–3198 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Corona, D. F., Clapier, C. R., Becker, P. B. & Tamkun, J. W. Modulation of ISWI function by site-specific histone acetylation. EMBO Rep. 3, 242–247 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Deng, H. et al. The JIL-1 kinase regulates the structure of Drosophila polytene chromosomes. Chromosoma 114, 173–182 (2005).

    Article  CAS  PubMed  Google Scholar 

  28. Meyer, B. J., McDonel, P., Csankovszki, G. & Ralston, E. Sex and X-chromosome-wide repression in Caenorhabditis elegans. Cold Spring Harb. Symp. Quant. Biol. 69, 71–79 (2004).

    Article  CAS  PubMed  Google Scholar 

  29. Chu, D. S. et al. A molecular link between gene-specific and chromosome-wide transcriptional repression. Genes Dev. 16, 796–805 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Bai, X., Alekseyenko, A. A. & Kuroda, M. I. Sequence-specific targeting of MSL complex regulates transcription of the roX RNA genes. EMBO J. 23, 2853–2861 (2004).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Rattner, B. P. & Meller, V. H. Drosophila male-specific lethal 2 protein controls sex-specific expression of the roX genes. Genetics 166, 1825–1832 (2004).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Straub, T. et al. Stable chromosomal association of MSL2 defines a dosage-compensated nuclear compartment. Chromosoma 114, 352–364 (2005).

    Article  PubMed  Google Scholar 

  33. Li, F., Parry, D. A. & Scott, M. J. The amino-terminal region of Drosophila MSL1 contains basic, glycine-rich, and leucine zipper-like motifs that promote X chromosome binding, self-association, and MSL2 binding, respectively. Mol. Cell. Biol. 25, 8913–8924 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Buscaino, A., Legube, G. & Akhtar, A. X-chromosome targeting and dosage compensation are mediated by distinct domains in MSL-3. EMBO Rep. 7, 531–538 (2006).

    CAS  PubMed  PubMed Central  Google Scholar 

  35. Morales, V. et al. Functional integration of the histone acetyltransferase MOF into the dosage compensation complex. EMBO J. 23, 2258–2268 (2004).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Morales, V., Regnard, C., Izzo, A., Vetter, I. & Becker, P. B. The MRG domain mediates the functional integration of MSL3 into the dosage compensation complex. Mol. Cell. Biol. 25, 5947–5954 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Akhtar, A. & Becker, P. B. Activation of transcription through histone H4 acetylation by MOF, an acetyltransferase essential for dosage compensation in Drosophila. Mol. Cell 5, 367–375 (2000).

    Article  CAS  PubMed  Google Scholar 

  38. Buscaino, A. et al. MOF-regulated acetylation of MSL-3 in the Drosophila dosage compensation complex. Mol. Cell 11, 1265–1277 (2003).

    Article  CAS  PubMed  Google Scholar 

  39. Smith, E. R. et al. A human protein complex homologous to the Drosophila MSL complex is responsible for the majority of histone H4 acetylation at lysine 16. Mol. Cell. Biol. 25, 9175–9188 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Taipale, M. et al. hMOF histone acetyltransferase is required for histone H4 lysine 16 acetylation in mammalian cells. Mol. Cell. Biol. 25, 6798–6810 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Gupta, A. et al. Involvement of human MOF in ATM function. Mol. Cell. Biol. 25, 5292–5305 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Stuckenholz, C., Meller, V. H. & Kuroda, M. I. Functional redundancy within roX1, a noncoding RNA involved in dosage compensation in Drosophila melanogaster. Genetics 164, 1003–1014 (2003).

    CAS  PubMed  PubMed Central  Google Scholar 

  43. Deng, X., Rattner, B. P., Souter, S. & Meller, V. H. The severity of roX1 mutations is predicted by MSL localization on the X chromosome. Mech. Dev. 122, 1094–1105 (2005).

    Article  CAS  PubMed  Google Scholar 

  44. Meller, V. H. Initiation of dosage compensation in Drosophila embryos depends on expression of the roX RNAs. Mech. Dev. 120, 759–767 (2003).

    Article  CAS  PubMed  Google Scholar 

  45. Lerach, S. et al. JIL-1 kinase, a member of the male-specific lethal (MSL) complex, is necessary for proper dosage compensation of eye pigmentation in Drosophila. Genesis 43, 213–215 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Ebert, A. et al. Su(var) genes regulate the balance between euchromatin and heterochromatin in Drosophila. Genes Dev. 18, 2973–2983 (2004).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Spierer, A., Seum, C., Delattre, M. & Spierer, P. Loss of the modifiers of variegation Su(var)3-7 or HP1 impacts male X polytene chromosome morphology and dosage compensation. J. Cell Sci. 118, 5047–5057 (2005).

    Article  CAS  PubMed  Google Scholar 

  48. Delattre, M., Spierer, A., Jaquet, Y. & Spierer, P. Increased expression of Drosophila Su(var)3-7 triggers Su(var)3-9-dependent heterochromatin formation. J. Cell Sci. 117, 6239–6247 (2004).

    Article  CAS  PubMed  Google Scholar 

  49. Mendjan, S. et al. Nuclear pore components are involved in the transcriptional regulation of dosage compensation in Drosophila. Mol. Cell 21, 811–823 (2006). The identification of novel interactors of the MOF acetyl transferase uncovers an important role for nuclear pores in D. melanogaster dosage compensation.

    Article  CAS  PubMed  Google Scholar 

  50. Dou, Y. et al. Physical association and coordinate function of the H3 K4 methyltransferase MLL1 and the H4 K16 acetyltransferase MOF. Cell 121, 873–885 (2005).

    Article  CAS  PubMed  Google Scholar 

  51. Taddei, A. et al. Nuclear pore association confers optimal expression levels for an inducible yeast gene. Nature 441, 774–778 (2006).

    Article  CAS  PubMed  Google Scholar 

  52. Cabal, G. G. et al. SAGA interacting factors confine sub-diffusion of transcribed genes to the nuclear envelope. Nature 441, 770–773 (2006).

    Article  CAS  PubMed  Google Scholar 

  53. Chaumeil, J., Le Baccon, P., Wutz, A. & Heard, E. A novel role for Xist RNA in the formation of a repressive nuclear compartment into which genes are recruited when silenced. Genes Dev. 20, 2223–2237 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Straub, T., Dahlsveen, I. K. & Becker, P. B. Dosage compensation in flies: mechanism, models, mystery. FEBS Lett. 579, 3258–3263 (2005).

    Article  CAS  PubMed  Google Scholar 

  55. Nusinow, D. A. & Panning, B. Recognition and modification of seX chromosomes. Curr. Opin. Genet. Dev. 15, 206–213 (2005).

    Article  CAS  PubMed  Google Scholar 

  56. Csankovszki, G., McDonel, P. & Meyer, B. J. Recruitment and spreading of the C. elegans dosage compensation complex along X chromosomes. Science 303, 1182–1185 (2004). A two-step process of binding and spreading operates to cover the worm X chromosome with DCC.

    Article  CAS  PubMed  Google Scholar 

  57. Heard, E. Delving into the diversity of facultative heterochromatin: the epigenetics of the inactive X chromosome. Curr. Opin. Genet. Dev. 15, 482–489 (2005).

    Article  CAS  PubMed  Google Scholar 

  58. Russell, L. B. Mammalian X chromosome action: inactivation limited in spread and region of origin. Science 140, 976–978 (1963).

    Article  CAS  Google Scholar 

  59. Popova, B. C., Tada, T., Takagi, N., Brockdorff, N. & Nesterova, T. B. Attenuated spread of X-inactivation in an X;autosome translocation. Proc. Natl Acad. Sci. USA 103, 7706–7711 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Lyon, M. F. The Lyon and the LINE hypothesis. Semin. Cell Dev. Biol. 14, 313–318 (2003).

    Article  CAS  PubMed  Google Scholar 

  61. Carrel, L. & Willard, H. F. X-inactivation profile reveals extensive variability in X-linked gene expression in females. Nature 434, 400–404 (2005). A chromosome-wide analysis of genes that escape X-chromosome inactivation in humans. The distribution of escapers along the chromosome correlates with its evolutionary history.

    Article  CAS  PubMed  Google Scholar 

  62. Fagegaltier, D. & Baker, B. S. X chromosome sites autonomously recruit the dosage compensation complex in Drosophila males. PLoS Biol. 2, e341 (2004).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  63. Oh, H., Bai, X., Park, Y., Bone, J. R. & Kuroda, M. I. Targeting dosage compensation to the X chromosome of Drosophila males. Cold Spring Harb. Symp. Quant. Biol. 69, 81–88 (2004).

    Article  CAS  PubMed  Google Scholar 

  64. Dahlsveen, I. K., Gilfillan, G. D., Shelest, V. I., Lamm, R. & Becker, P. B. Targeting determinants of dosage compensation in Drosophila. PLoS Genet. 2, e5 (2006).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  65. Demakova, O. V. et al. The MSL complex levels are critical for its correct targeting to the chromosomes in Drosophila melanogaster. Chromosoma 112, 103–115 (2003).

    Article  CAS  PubMed  Google Scholar 

  66. Mockler, T. C. et al. Applications of DNA tiling arrays for whole-genome analysis. Genomics 85, 1–15 (2005).

    Article  CAS  PubMed  Google Scholar 

  67. Park, Y. et al. et al. Sequence-specific targeting of Drosophila roX genes by the MSL dosage compensation complex. Mol. Cell 11, 977–986 (2003).

    Article  CAS  PubMed  Google Scholar 

  68. Singh, N. D., Davis, J. C. & Petrov, D. A. Codon bias and noncoding GC content correlate negatively with recombination rate on the Drosophila X chromosome. J. Mol. Evol. 61, 315–324 (2005).

    Article  CAS  PubMed  Google Scholar 

  69. Sass, G. L., Pannuti, A. & Lucchesi, J. C. Male-specific lethal complex of Drosophila targets activated regions of the X chromosome for chromatin remodeling. Proc. Natl Acad. Sci. USA 100, 8287–8291 (2003). This is the only study so far that shows directly that the D. melanogaster DCC can be recruited de novo following transcription activation.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  70. Saunders, A., Leighton, J. C. & Lis, J. T. Breaking barriers to transcription elongation. Nature Rev. Mol. Cell Biol. 7, 557–567 (2006).

    Article  CAS  Google Scholar 

  71. Sims, R. J. 3rd, Belotserkovskaya, R. & Reinberg, D. Elongation by RNA polymerase II: the short and long of it. Genes Dev. 18, 2437–2468 (2004).

    Article  CAS  PubMed  Google Scholar 

  72. Kageyama, Y. et al. Association and spreading of the Drosophila dosage compensation complex from a discrete roX1 chromatin entry site. EMBO J. 20, 2236–2245 (2001).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  73. Oh, H., Bone, J. R. & Kuroda, M. I. Multiple classes of MSL binding sites target dosage compensation to the X chromosome of Drosophila. Curr. Biol. 14, 481–487 (2004).

    Article  CAS  PubMed  Google Scholar 

  74. Kotlikova, I. V. et al. The Drosophila dosage compensation complex binds to polytene chromosomes independently of developmental changes in transcription. Genetics 172, 963–974 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  75. Gu, W., Wei, X., Pannuti, A. & Lucchesi, J. C. Targeting the chromatin remodeling MSL complex of Drosophila to its sites of action on the X chromosome requires both acetyl transferase and ATPase activities. EMBO J. 19, 5202–5211 (2000).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  76. Mito, Y., Henikoff, J. G. & Henikoff, S. Genome-scale profiling of histone H3.3 replacement patterns. Nature Genet. 37, 1090–1097 (2005).

    Article  CAS  PubMed  Google Scholar 

  77. Kristjuhan, A. & Svejstrup, J. Q. Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo. EMBO J. 23, 4243–4252 (2004).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  78. O'Sullivan, J. M. et al. Gene loops juxtapose promoters and terminators in yeast. Nature Genet. 36, 1014–1018 (2004).

    Article  CAS  PubMed  Google Scholar 

  79. Hagstrom, K. A. & Meyer, B. J. Condensin and cohesin: more than chromosome compactor and glue. Nature Rev. Genet. 4, 520–534 (2003).

    Article  CAS  PubMed  Google Scholar 

  80. Krogan, N. J. et al. COMPASS, a histone H3 (Lysine 4) methyltransferase required for telomeric silencing of gene expression. J. Biol. Chem. 277, 10753–10755 (2002).

    Article  CAS  PubMed  Google Scholar 

  81. Roguev, A. et al. The Saccharomyces cerevisiae Set1 complex includes an Ash2 homologue and methylates histone 3 lysine 4. EMBO J. 20, 7137–7148 (2001).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  82. McDonel, P., Jans, J., Peterson, B. K. & Meyer, B. J. Clustered DNA motifs mark X chromosomes for repression by a dosage compensation complex. Nature 19 November 2006 (doi:10.1038/nature05338).

Download references

Acknowledgements

Research on dosage compensation in P.B.B.'s laboratory is supported by the Deutsche Forschungsgemeinschaft through Transregio 5 and the Leibniz Programme. Additional support from the Network of Excellence, 'The Epigenome', funded by the 6th Framework Programme of the European Union is also appreciated. We thank I. Dahlsveen for the immunofluorescence image shown in Figure 3.

Author information

Authors and Affiliations

  1. Department of Molecular Biology, Adolf Butenandt Institute, Ludwig Maximilians University, Munich, 80336, Germany

    Tobias Straub & Peter B. Becker

Authors
  1. Tobias Straub
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Peter B. Becker
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Peter B. Becker.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Related links

Related links

DATABASES

WormBase

DPY-21

DPY-26

DPY-27

DPY-28

DPY-30

her-1

MIX-1

FURTHER INFORMATION

Peter B. Becker's homepage

Glossary

Heterochromatin

A condensed and transcriptionally silent form of chromatin that is found at telomeres and centromeres of all chromosomes. Heterochromatin components, such as heterochromatin protein 1 (HP1), can be recruited to contribute to gene repression in general.

Hemizygosity

When a diploid genotype has only one copy of a particular gene, as in X-chromosomal genes in human and Drosophila melanogaster males, or when the homologous chromosome is lost or carries a deletion.

Haploinsufficiency

A gene dosage effect that occurs when a diploid organism requires both functional copies of a gene for a wild-type phenotype.

Monosomy

The lack of a counterpart for an entire chromosome.

Polycomb group

A set of developmental transcription repressors that interact to silence genes in an epigenetically stable manner involving histone methylation marks.

30 nm fibre

A chromatin fibre with a diameter of roughly 30 nm, which originates from the folding of the nucleosomal array.

Polytene chromosomes

Specialized interphase chromosomes of the Drosophila melanogaster salivary gland, which consist of about 1,000 identical chromatids lined up together. DNA staining reveals a pattern of gene-poor, condensed 'bands' that are separated by decondensed, gene-rich interbands.

Epigenetic

Any heritable change in gene expression that is not caused by a change in DNA sequence.

LINE-1

Long interspersed nuclear element. This is a family of mammalian retrotransposons of high abundance (for example, the human genome contains about 900,000 LINEs, covering about 20% of the genome).

ChIP-on-chip analysis

A powerful method to map the distribution of chromatin proteins along genomes by chromatin immunoprecipitation (ChIP) and subsequent hybridization of the co-precipitated DNA to oligonucleotide microarrays (chip).

Codon bias

The preference for specific codons over others that code for the same amino acid.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Straub, T., Becker, P. Dosage compensation: the beginning and end of generalization. Nat Rev Genet 8, 47–57 (2007). https://doi.org/10.1038/nrg2013

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrg2013

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing