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¹ Human Cytogenetics Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, England, UK
² Centre for Structural Biology, Department of Biological Sciences, Imperial College London, London SW7 2AZ, England, UK
³ Structural Bioinformatics Group, Department of Biological Sciences, Imperial College London, London SW7 2AZ, England, UK
⁴ Department of Epidemiology, Mathematics, and Statistics, Cancer Research UK, Wolfson Institute of Preventive Medicine, London EC1M 6BQ, England, UK

Address correspondence to Denise Sheer, Human Cytogenetics Laboratory, Cancer Research UK, London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, England, UK. Tel.: 44-20-7269-3220. Fax: 44-20-7269-3655. email: denise.sheer{at}cancer.org.uk; or Paul Freemont, Centre for Structural Biology, Department of Biological Sciences, Imperial College London, South Kensington Campus, London SW7 2AZ, England, UK. Tel.: 44-20-7594-5327. Fax: 44-20-7594-3057. email: p.freemont{at}imperial.ac.uk

The promyelocytic leukemia (PML) protein is aggregated into nuclear bodies that are associated with diverse nuclear processes. Here, we report that the distance between a locus and its nearest PML body correlates with the transcriptional activity and gene density around the locus. Genes on the active X chromosome are more significantly associated with PML bodies than their silenced homologues on the inactive X chromosome. We also found that a histone-encoding gene cluster, which is transcribed only in S-phase, is more strongly associated with PML bodies in S-phase than in G0/G1 phase of the cell cycle. However, visualization of specific RNA transcripts for several genes showed that PML bodies were not themselves sites of transcription for these genes. Furthermore, knock-down of PML bodies by RNA interference did not preferentially change the expression of genes closely associated with PML bodies. We propose that PML bodies form in nuclear compartments of high transcriptional activity, but they do not directly regulate transcription of genes in these compartments.

Key Words: PML nuclear body; major histocompatibility complex; transcription; gene density; nuclear organization

Abbreviations used in this paper: APL, acute promyelocytic leukemia; ATRA, all-trans retinoic acid; CBP, cAMP-response element binding protein; MHC, major histocompatibility complex; mmd, mean minimum distance; PML, promyelocytic leukemia; RNAi, RNA interference; SiRNA, small-interfering RNA; TAP/LMP, transporter associated with antigen processing/large multifunctional protease.

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