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:

Nuclear compartmentalization and gene activity

Abstract

The regulated expression of genes during development and differentiation is influenced by the availability of regulatory proteins and accessibility of the DNA to the transcriptional apparatus. There is growing evidence that the transcriptional activity of genes is influenced by nuclear organization, which itself changes during differentiation. How do these changes in nuclear organization help to establish specific patterns of gene expression?

Key Points

  • During cellular differentiation, only specific subsets of genes are required to carry out a cell's specialized function. The remainder are silenced. Inactive regions of the chromosome are packaged into transcriptionally inactive heterochromatin, mediated by histone deactylation; these regions are unique to each differentiated cell type.

  • Gene potentiation is a prerequisite to gene activation. This opens the chromatin structure so that DNA is accessible to the activator proteins required for transcription. Histone acetylation is required to mediate this chromatin opening.

  • Chromosomes and genes are organized into specific nuclear zones, termed chromosome territories; within this, potentially active regions are located at the periphery. These territories occupy non-random positions in the interphase nucleus, specific to each cell type. Changes in nuclear architecture are proposed to occur during differentiation.

  • Nuclear functions such as transcription also occur in specific compartments of the nucleus. Therefore, nuclear architecture may allow active genes to localize to regions that are permissive for transcription.

  • Evidence from Drosophila melanogaster and mammals indicates that positioning of a gene near centromeric heterochromatin often promotes gene silencing; and likewise, that sequestration of a gene into a permissive compartment often allows the stably inherited chromatin opening of a locus.

  • Modification of chromatin structure over large regions is proposed to be initiated by assembly of proteins on cis-acting elements called silencer elements. Proteins that bind to these elements include Sir proteins in yeast, and the Polycomb proteins in Drosophila. This repressive structure is proposed to propagate along the chromosome.

  • Studies indicate that enhancer elements can counteract these silencing events. Binding of enhancer elements is proposed to recruit the gene to a region in the nucleus that is rich in the transcription factors and histone acetylases required to activate transcription.

  • Cancer is associated with disruption of gene expression patterns and global disorganization of chromosome organization within the nucleus.

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

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

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

Figure 1: Patterns of chromatin condensation in haematopoietic cells.
Figure 2: Chromatin condensation accompanies cellular differentiation.
Figure 3: Chromatin structure and gene expression.
Figure 4: Fluorescence in situ hybridization to study gene localization.
Figure 5: Activation at the β-globin locus: a multistep process?

Similar content being viewed by others

References

  1. John, B. The Biology of Heterochromatin (ed. Verma, R. S.) (Cambridge Univ. Press, Cambridge, 1988).

    Google Scholar 

  2. Leitch, A. R. Higher levels of organization in the interphase nucleus of cycling and differentiated cells. Microbiol. Mol. Biol. Rev. 64, 138 ?152 (2000).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Felsenfeld, G. Chromatin as an essential part of the transcriptional mechanism. Nature 355, 219?224 ( 1992).

    Article  CAS  PubMed  Google Scholar 

  4. Gregory, P. D. & Horz, W. Chromatin and transcription ? how transcription factors battle with a repressive chromatin environment. Eur. J. Biochem. 251, 9?18 (1998).

    Article  CAS  PubMed  Google Scholar 

  5. Kadonaga, J. T. Eukaryotic transcription: An interlaced network of transcription factors and chromatin-modifying machines. Cell 92, 307 ?313 (1998).

    Article  CAS  PubMed  Google Scholar 

  6. Wolffe, A. P. Transcription: In tune with the histones. Cell 77, 13?16 (1994).

    Article  CAS  PubMed  Google Scholar 

  7. Kramer, J. A., McCarrey, J. R., Djakiew, D. & Krawetz, S. A. Differentiation: The selective potentiation of chromatin domains. Development 125, 4749?4755 (1998).

    CAS  PubMed  Google Scholar 

  8. Jimenez, G., Griffiths, S. D., Ford, A. M., Greaves, M. F. & Enver, T. Activation of the β-globin locus control region precedes commitment to the erythroid lineage. Proc. Natl Acad. Sci. USA 89, 10618?10622 (1992).

    Article  CAS  PubMed  Google Scholar 

  9. Hu, M. et al. Multilineage gene expression precedes commitment in the hemopoietic system. Genes Dev. 11, 774? 785 (1997).

    Article  CAS  PubMed  Google Scholar 

  10. Lee, D. Y., Hayes, J. J., Pruss, D. & Wolffe, A. P. A positive role for histone acetylation in transcription factor access to nucleosomal DNA . Cell 72, 73?84 (1993).

    Article  CAS  PubMed  Google Scholar 

  11. Wolffe, A. P. & Pruss, D. Targeting chromatin disruption: Transcription regulators that acetylate histones. Cell 84, 817?819 (1996).

    Article  CAS  PubMed  Google Scholar 

  12. Turner, B. M. Histone acetylation as an epigenetic determinant of long-term transcriptional competence. Cell. Mol. Life Sci. 54, 21? 31 (1998).

    Article  CAS  PubMed  Google Scholar 

  13. Wolffe, A. P. Packaging principle: How DNA methylation and histone acetylation control the transcriptional activity of chromatin. J. Exp. Zool. 282, 239?244 (1998).

    Article  CAS  PubMed  Google Scholar 

  14. Crane-Robinson, C. How do linker histones mediate differential gene expression? Bioessays 21, 367?371 ( 1999).

    Article  CAS  PubMed  Google Scholar 

  15. Wolffe, A. P., Khochbin, S. & Dimitrov, S. What do linker histones do in chromatin? Bioessays 19, 249?255 ( 1997).

    Article  CAS  PubMed  Google Scholar 

  16. Keohane, A. M., O'Neill L, P., Belyaev, N. D., Lavender, J. S. & Turner, B. M. X-inactivation and histone H4 acetylation in embryonic stem cells. Dev. Biol. 180 , 618?630 (1996).

    Article  CAS  PubMed  Google Scholar 

  17. Vyas, P. et al. Cis-acting sequences regulating expression of the human α-globin cluster lie within constitutively open chromatin. Cell 69, 781?793 (1992).

    Article  CAS  PubMed  Google Scholar 

  18. O'Neill, L. P. & Turner, B. M. Histone H4 acetylation distinguishes coding regions of the human genome from heterochromatin in a differentiation-dependent but transcription-independent manner. EMBO J. 14, 3946?3957 ( 1995).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Schübeler, D. et al. Nuclear localization and histone acetylation: A pathway for chromatin opening and transcriptional activation of the human β-globin locus. Genes Dev. 14, 940? 950 (2000).Indicates that positioning away from the heterochromatin compartment may mediate open chromatin configuration and histone acetylation of the human globin locus.

    PubMed  PubMed Central  Google Scholar 

  20. Reddy, P. M. & Shen, C. K. Erythroid differentiation of mouse erythroleukemia cells results in reorganization of protein?DNA complexes in the mouse β-major globin promoter but not its distal enhancer. Mol. Cell. Biol. 13, 1093?1103 (1993).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Cohen, R. B. & Sheffery, M. Nucleosome disruption precedes transcription and is largely limited to the transcribed domain of globin genes in murine erythroleukemia cells. J. Mol. Biol. 182, 109?129 (1985).

    Article  CAS  PubMed  Google Scholar 

  22. Benezra, R., Cantor, C. R. & Axel, R. Nucleosomes are phased along the mouse β-major globin gene in erythroid and nonerythroid cells. Cell 44, 697?704 (1986).

    Article  CAS  PubMed  Google Scholar 

  23. Sheffery, M., Rifkind, R. A. & Marks, P. A. Murine erythroleukemia cell differentiation: DNase I hypersensitivity and DNA methylation near the globin genes. Proc. Natl Acad. Sci. USA 79, 1180? 1184 (1982).

    Article  CAS  PubMed  Google Scholar 

  24. Lamond, A. I. & Earnshaw, W. C. Structure and function in the nucleus. Science 280, 547? 553 (1998).

    Article  CAS  PubMed  Google Scholar 

  25. Cockell, M. & Gasser, S. M. Nuclear compartments and gene regulation. Curr. Opin. Genet. Dev. 9, 199 ?205 (1999).

    Article  CAS  PubMed  Google Scholar 

  26. Marshall, W. F., Fung, J. C. & Sedat, J. W. Deconstructing the nucleus: Global architecture from local interactions. Curr. Opin. Genet. Dev. 7, 259?263 (1997).

    Article  CAS  PubMed  Google Scholar 

  27. Munkel, C. et al. Compartmentalization of interphase chromosomes observed in simulation and experiment. J. Mol. Biol. 285, 1053?1065 (1999).

    Article  CAS  PubMed  Google Scholar 

  28. Manuelidis, L. A view of interphase chromosomes. Science 250, 1533?1540 (1990).

    Article  CAS  PubMed  Google Scholar 

  29. Zink, D. et al. Structure and dynamics of human interphase chromosome territories in vivo. Hum. Genet. 102, 241? 251 (1998).

    Article  CAS  PubMed  Google Scholar 

  30. Manuelidis, L. Different central nervous system cell types display distinct and nonrandom arrangements of satellite DNA sequences. Proc. Natl Acad. Sci. USA 81, 3123?3127 ( 1984).One of the first papers showing that the spatial organization of centromeres is non-random and cell-type specific, and indicating that this could represent specific functional capacities.

    Article  CAS  PubMed  Google Scholar 

  31. Manuelidis, L. & Borden, J. Reproducible compartmentalization of individual chromosome domains in human CNS cells revealed by in situ hybridization and three-dimensional reconstruction. Chromosoma 96, 397?410 ( 1988).

    Article  CAS  PubMed  Google Scholar 

  32. Haaf, T. & Schmid, M. Chromosome topology in mammalian interphase nuclei. Exp. Cell Res. 192, 325 ?332 (1991).

    Article  CAS  PubMed  Google Scholar 

  33. Sadoni, N. et al. Nuclear organization of mammalian genomes. Polar chromosome territories build up functionally distinct higher order compartments. J. Cell Biol. 146, 1211?1226 (1999).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Park, P. C. & De Boni, U. Transposition of DNase hypersensitive chromatin to the nuclear periphery coincides temporally with nerve growth factor-induced up-regulation of gene expression in PC12 cells. Proc. Natl Acad. Sci. USA 93, 11646? 11651 (1996).

    Article  CAS  PubMed  Google Scholar 

  35. de Graaf, A. et al. Three-dimensional distribution of DNase I-sensitive chromatin regions in interphase nuclei of embryonal carcinoma cells. Eur. J. Cell Biol. 52, 135?141 (1990).

    CAS  PubMed  Google Scholar 

  36. Croft, J. A. et al. Differences in the localization and morphology of chromosomes in the human nucleus. J. Cell Biol. 145, 1119?1131 (1999). Analyses the influence of the cell cycle and the inhibition of transcription on the morphology and distribution of specific human chromosome territories.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Kurz, A. et al. Active and inactive genes localize preferentially in the periphery of chromosome territories. J. Cell Biol. 135, 1195?1205 (1996).

    Article  CAS  PubMed  Google Scholar 

  38. Verschure, P. J., van Der Kraan, I., Manders, E. M. & van Driel, R. Spatial relationship between transcription sites and chromosome territories . J. Cell Biol. 147, 13? 24 (1999).Shows that transcription is compartmentalized, and that sites of active transcription are distinct from sites of inactive chromatin.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  39. Zirbel, R. M., Mathieu, U. R., Kurz, A., Cremer, T. & Lichter, P. Evidence for a nuclear compartment of transcription and splicing located at chromosome domain boundaries. Chromosome Res. 1, 93?106 ( 1993).

    Article  CAS  PubMed  Google Scholar 

  40. Volpi, E. V. et al. Large-scale chromatin organization of the major histocompatibility complex and other regions of human chromosome 6 and its response to interferon in interphase nuclei. J. Cell Sci. 113, 1565?1576 (2000). This paper finds a correlation between the formation of large external chromatin loops, outside a chromosome territory, and the transcriptional activity of a gene cluster.

    CAS  PubMed  Google Scholar 

  41. Grande, M. A., van der Kraan, I., de Jong, L. & van Driel, R. Nuclear distribution of transcription factors in relation to sites of transcription and RNA polymerase II. J. Cell Sci. 110, 1781?1791 (1997).

    CAS  PubMed  Google Scholar 

  42. Pombo, A. et al. Regional and temporal specialization in the nucleus: A transcriptionally active nuclear domain rich in PTF, Oct1 and PIKA antigens associates with specific chromosomes early in the cell cycle. EMBO J. 17, 1768?1778 (1998).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. van Steensel, B. et al. Partial colocalization of glucocorticoid and mineralocorticoid receptors in discrete compartments in nuclei of rat hippocampus neurons. J. Cell Sci. 109, 787?792 (1996).

    CAS  PubMed  Google Scholar 

  44. Aagaard, L. et al. Functional mammalian homologues of the Drosophila PEV-modifier Su(var)3-9 encode centromere-associated proteins which complex with the heterochromatin component M31. EMBO J. 18, 1923?1938 (1999).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. Brown, K. E. et al. Association of transcriptionally silent genes with Ikaros complexes at centromeric heterochromatin. Cell 91, 845?854 (1997).Ikaros, a protein associated with heterochromatin foci in the nucleus of mouse B lymphocytes, is also associated with transcriptionally inactive genes, indicating a different mechanism for gene silencing.

    Article  CAS  PubMed  Google Scholar 

  46. Wreggett, K. A. et al. A mammalian homologue of Drosophila heterochromatin protein 1 (HP1) is a component of constitutive heterochromatin. Cytogenet. Cell Genet. 66, 99?103 (1994).

    Article  CAS  PubMed  Google Scholar 

  47. Hendrich, B. & Bird, A. Identification and characterization of a family of mammalian methyl-CpG binding proteins. Mol. Cell. Biol. 18, 6538?6547 ( 1998).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  48. Lewis, J. D. et al. Purification, sequence, and cellular localization of a novel chromosomal protein that binds to methylated DNA. Cell 69, 905?914 (1992).

    Article  CAS  PubMed  Google Scholar 

  49. Kim, J. et al. Ikaros DNA-binding proteins direct formation of chromatin remodeling complexes in lymphocytes. Immunity 10, 345 ?355 (1999).Ikaros can recruit histone deacetylases and chromatin remodelling complexes to regions of heterochromatin in the nucleus of mouse T lymphocytes.

    Article  CAS  PubMed  Google Scholar 

  50. Shelby, R. D., Hahn, K. M. & Sullivan, K. F. Dynamic elastic behavior of α-satellite DNA domains visualized in situ in living human cells. J. Cell Biol. 135, 545?557 ( 1996).

    Article  CAS  PubMed  Google Scholar 

  51. Vourc'h, C., Taruscio, D., Boyle, A. L. & Ward, D. C. Cell cycle-dependent distribution of telomeres, centromeres, and chromosome-specific subsatellite domains in the interphase nucleus of mouse lymphocytes. Exp. Cell Res. 205, 142?151 (1993).

    Article  CAS  PubMed  Google Scholar 

  52. Alcobia, I., Dilao, R. & Parreira, L. Spatial associations of centromeres in the nuclei of hematopoietic cells: Evidence for cell-type-specific organizational patterns . Blood 95, 1608?1615 (2000).

    CAS  PubMed  Google Scholar 

  53. Manuelidis, L. Indications of centromere movement during interphase and differentiation. Ann. NY Acad. Sci. 450, 205?221 (1985).

    Article  CAS  PubMed  Google Scholar 

  54. Minc, E., Allory, Y., Worman, H. J., Courvalin, J. C. & Buendia, B. Localization and phosphorylation of HP1 proteins during the cell cycle in mammalian cells. Chromosoma 108, 220?234 ( 1999).

    Article  CAS  PubMed  Google Scholar 

  55. Kozubek, S. et al. Distribution of ABL and BCR genes in cell nuclei of normal and irradiated lymphocytes. Blood 89, 4537 ?4545 (1997).

    CAS  PubMed  Google Scholar 

  56. Neves, H., Ramos, C., da Silva, M. G., Parreira, A. & Parreira, L. The nuclear topography of ABL, BCR, PML, and RARαgenes: Evidence for gene proximity in specific phases of the cell cycle and stages of hematopoietic differentiation. Blood 93, 1197?1207 ( 1999).

    CAS  PubMed  Google Scholar 

  57. Bartova, E. et al. Nuclear topography of the c -myc gene in human leukemic cells. Gene 244, 1?11 (2000).

    Article  CAS  PubMed  Google Scholar 

  58. Bridger, J. M., Boyle, S., Kill, I. R. & Bickmore, W. A. Re-modelling of nuclear architecture in quiescent and senescent human fibroblasts. Curr. Biol. 10, 149?152 (2000).

    Article  CAS  PubMed  Google Scholar 

  59. Tang, Q. Q. & Lane, M. D. Activation and centromeric localization of CCAAT/enhancer-binding proteins during the mitotic clonal expansion of adipocyte differentiation. Genes Dev. 13, 2231?2241 (1999).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Dernburg, A. F. et al. Perturbation of nuclear architecture by long-distance chromosome interactions. Cell 85, 745? 759 (1996).

    Article  CAS  PubMed  Google Scholar 

  61. Csink, A. K. & Henikoff, S. Large-scale chromosomal movements during interphase progression in Drosophila. J. Cell Biol. 143, 13?22 ( 1998).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  62. Csink, A. K. & Henikoff, S. Genetic modification of heterochromatic association and nuclear organization in Drosophila. Nature 381, 529?531 ( 1996).

    Article  CAS  PubMed  Google Scholar 

  63. Brown, K. E., Baxter, J., Graf, D., Merkenschlager, M. & Fisher, A. G. Dynamic repositioning of genes in the nucleus of lymphocytes preparing for cell division. Mol. Cell 3, 207?217 (1999).

    Article  CAS  PubMed  Google Scholar 

  64. Aparicio, O. M., Billington, B. L. & Gottschling, D. E. Modifiers of position effect are shared between telomeric and silent mating-type loci in S. cerevisiae. Cell 66, 1279?1287 (1991).

    Article  CAS  PubMed  Google Scholar 

  65. Chien, C. T., Buck, S., Sternglanz, R. & Shore, D. Targeting of SIR1 protein establishes transcriptional silencing at HM loci and telomeres in yeast. Cell 75, 531?541 (1993).

    Article  CAS  PubMed  Google Scholar 

  66. Gotta, M. & Gasser, S. M. Nuclear organization and transcriptional silencing in yeast. Experientia 52, 1136 ?1147 (1996).

    Article  CAS  PubMed  Google Scholar 

  67. Laroche, T. et al. Mutation of yeast Ku genes disrupts the subnuclear organization of telomeres. Curr. Biol. 8, 653?656 (1998).

    Article  CAS  PubMed  Google Scholar 

  68. Maillet, L. et al. Evidence for silencing compartments within the yeast nucleus: A role for telomere proximity and Sir protein concentration in silencer-mediated repression. Genes Dev. 10, 1796? 1811 (1996).

    Article  CAS  PubMed  Google Scholar 

  69. Andrulis, E. D., Neiman, A. M., Zappulla, D. C. & Sternglanz, R. Perinuclear localization of chromatin facilitates transcriptional silencing Nature 394, 592?595 (1998).

    Article  CAS  PubMed  Google Scholar 

  70. Francastel, C., Walters, M. C., Groudine, M. & Martin, D. I. A functional enhancer suppresses silencing of a transgene and prevents its localization close to centrometric heterochromatin. Cell 99, 259?269 (1999). Stable transgene expression requires positioning away from the heterochromatin compartment and the binding of transcription factors to the enhancer.

    Article  CAS  PubMed  Google Scholar 

  71. Bulger, M. & Groudine, M. Looping versus linking: Toward a model for long-distance gene activation. Genes Dev. 13, 2465?2477 (1999).

    Article  CAS  PubMed  Google Scholar 

  72. Lustig, A. J. Mechanisms of silencing in Saccharomyces cerevisiae. Curr. Opin. Genet. Dev. 8, 233?239 (1998).

    Article  CAS  PubMed  Google Scholar 

  73. Moehrle, A. & Paro, R. Spreading the silence: epigenetic transcriptional regulation during Drosophila development. Dev. Genet. 15, 478?484 (1994).

    Article  CAS  PubMed  Google Scholar 

  74. Loo, S. & Rine, J. Silencing and heritable domains of gene expression. Annu. Rev. Cell Dev. Biol. 11, 519?548 (1995).

    Article  CAS  PubMed  Google Scholar 

  75. Aparicio, O. M. & Gottschling, D. E. Overcoming telomeric silencing: a trans-activator competes to establish gene expression in a cell cycle-dependent way. Genes Dev. 8, 1133?1146 (1994).

    Article  CAS  PubMed  Google Scholar 

  76. Festenstein, R. et al. Locus control region function and heterochromatin-induced position effect variegation. Science 271, 1123?1125 (1996).

    Article  CAS  PubMed  Google Scholar 

  77. Walters, M. C. et al. Transcriptional enhancers act in cis to suppress position-effect variagation. Genes Dev. 10, 185? 195 (1996).

    Article  CAS  PubMed  Google Scholar 

  78. Linares-Cruz, G. et al. p21WAF-1 reorganizes the nucleus in tumor suppression. Proc. Natl Acad. Sci. USA 95, 1131? 1135 (1998).Global disorganization of nuclear architecture can be associated with cancer, but is reversible during tumour suppression.

    Article  CAS  PubMed  Google Scholar 

  79. Qumsiyeh, M. B. Impact of rearrangements on function and position of chromosomes in the interphase nucleus and on human genetic disorders. Chromosome Res. 3, 455?465 (1995).

    Article  CAS  PubMed  Google Scholar 

  80. Epner, E. et al. The β-globin LCR is not necessary for an open chromatin structure or developmentally regulated transcription of the native mouse β-globin locus. Mol. Cell 2, 447? 455 (1998).

    Article  CAS  PubMed  Google Scholar 

  81. Reik, A. et al. The locus control region is necessary for gene expression in the human β?globin locus but not the maintenance of an open chromatin structure in erythroid cells. Mol. Cell. Biol. 18, 5992?6000 (1998).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  82. Rozman, C., Woessner, S., Feliu, E., Lafuente, R. & Berga, L. Cell Ultrastructure for Hematologists (ed. Ediciones Doyma, S. A.) (Barcelona, Spain, 1993).

    Google Scholar 

  83. Alberts, B. et al. Molecular Biology of the Cell 3rd edn (Garland, New York, 1994).

    Google Scholar 

Download references

Acknowledgements

The authors thank Matthew Lorincz and Bas van Steensel for their useful comments on this manuscript. This work was supported by a special fellowship to C.F. from the Leukemia and Lymphoma Society, a fellowship from the Deutsche Forschungsgemeinschaft to D.S., and NIH grants to M.G.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Mark Groudine.

Related links

Related links

ENCYCLOPEDIA OF LIFE SCIENCES

Nucleosomes: detailed structure and mutations

Glossary

HETEROCHROMATIN

A condensed form of chromatin; the degree of compaction is similar to that of mitotic chromosomes. It is usually found around the centromere.

INTERPHASE

The period between two mitotic divisions.

ENHANCERS

Increase transcription of a linked promoter if placed in either orientation, upstream or downstream.

EUCHROMATIN

Chromatin that appears less compact than mitotic chromosomes. Active genes are contained within euchromatin.

METHYL-DNA-BINDING DOMAIN PROTEINS

Proteins that bind specifically to methylated DNA through a methyl-DNA-binding domain. Some of these proteins are involved in transcriptional repression of methylated DNA.

SATELLITES

Relatively short DNA sequences that are highly repeated in long tandem arrays.

CONSTITUTIVE HETEROCHROMATIN

The fraction of heterochromatin that stays compact through the cell cycle. It is mainly composed of repetitive sequences (satellite DNA; see above), and is concentrated in characteristic regions such as centromeres.

CHROMOCENTRES

Aggregates of constitutive heterochromatin from different chromosomes.

SILENCER ELEMENTS

Cis-acting elements that are involved in silencing, most probably by directly recruiting repressive proteins.

LOCUS CONTROL REGION

Defined by its ability, in transgenic assays, to confer high-level, tissue-specific expression on a linked promoter, at all integration sites.

FACULTATIVE HETEROCHROMATIN

Fraction of chromatin that is condensed and inactive in a given cell lineage, which may be decondensed and active in another.

ANEUPLOIDY

The ploidy of a cell refers to the number of sets of chromosomes that it contains. Aneuploid karyotypes are those whose chromosome complements are not a simple multiple of the haploid set.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Francastel, C., Schübeler, D., Martin, D. et al. Nuclear compartmentalization and gene activity. Nat Rev Mol Cell Biol 1, 137–143 (2000). https://doi.org/10.1038/35040083

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1038/35040083

This article is cited by

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