DNA viruses and viral proteins that interact with PML nuclear bodies

Connections between PML nuclear bodies (PML NBs) and DNA virus replication have been investigated from the earliest days of the molecular characterization of PML and associated proteins. It appears to be a general feature of nuclear-replicating DNA viruses that their parental genomes preferentially become associated with PML NBs, and that their initial sites of transcription and development of DNA replication centres are frequently juxtaposed to these domains or their remnants. In addition, regulatory proteins encoded by several DNA viruses associate with and sometimes cause catastrophic changes to PML NBs by a variety of mechanisms. These events can be correlated with the efficiency of viral infection and the functions of viral regulatory proteins, but the underlying molecular connections between PML NB function and viral infection remain poorly understood. This article reviews the latest developments in the interactions between PML NBs and herpesviruses, adenoviruses and papovaviruses.

[1]  J. Lyle,et al.  A deletion mutant in the human cytomegalovirus gene encoding IE1(491aa) is replication defective due to a failure in autoregulation. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[2]  R. Everett,et al.  Nuclear domain 10 as preexisting potential replication start sites of herpes simplex virus type-1. , 1996, Virology.

[3]  S. Weller,et al.  Formation of herpes simplex virus type 1 replication compartments by transfection: requirements and localization to nuclear domain 10 , 1997, Journal of virology.

[4]  A. Weissman,et al.  RING Finger Proteins Mediators of Ubiquitin Ligase Activity , 2000, Cell.

[5]  E. Yeh,et al.  Pml Is Critical for Nd10 Formation and Recruits the Pml-Interacting Protein Daxx to This Nuclear Structure When Modified by Sumo-1 , 1999, The Journal of cell biology.

[6]  R. Everett,et al.  A novel ubiquitin‐specific protease is dynamically associated with the PML nuclear domain and binds to a herpesvirus regulatory protein , 1997, The EMBO journal.

[7]  G. Wilkinson,et al.  Disruption of PML-associated nuclear bodies during human cytomegalovirus infection. , 1995, The Journal of general virology.

[8]  G. Maul,et al.  The periphery of nuclear domain 10 (ND10) as site of DNA virus deposition , 1996, The Journal of cell biology.

[9]  P. Freemont,et al.  The Disruption of ND10 during Herpes Simplex Virus Infection Correlates with the Vmw110- and Proteasome-Dependent Loss of Several PML Isoforms , 1998, Journal of Virology.

[10]  R. Everett,et al.  Alphaherpesvirus Proteins Related to Herpes Simplex Virus Type 1 ICP0 Affect Cellular Structures and Proteins , 2000, Journal of Virology.

[11]  G. Hayward,et al.  The major immediate-early proteins IE1 and IE2 of human cytomegalovirus colocalize with and disrupt PML-associated nuclear bodies at very early times in infected permissive cells , 1997, Journal of virology.

[12]  K. Sullivan,et al.  Degradation of Nucleosome-associated Centromeric Histone H3-like Protein CENP-A Induced by Herpes Simplex Virus Type 1 Protein ICP0* , 2001, The Journal of Biological Chemistry.

[13]  M. Ballestas,et al.  Efficient persistence of extrachromosomal KSHV DNA mediated by latency-associated nuclear antigen. , 1999, Science.

[14]  N. Bastien,et al.  Interaction of the papillomavirus E2 protein with mitotic chromosomes. , 2000, Virology.

[15]  H. Hofmann,et al.  Covalent Modification of the Transactivator Protein IE2-p86 of Human Cytomegalovirus by Conjugation to the Ubiquitin-Homologous Proteins SUMO-1 and hSMT3b , 2000, Journal of Virology.

[16]  G. Maul,et al.  Review: properties and assembly mechanisms of ND10, PML bodies, or PODs. , 2000, Journal of structural biology.

[17]  W. Halford,et al.  ICP0 Is Required for Efficient Reactivation of Herpes Simplex Virus Type 1 from Neuronal Latency , 2001, Journal of Virology.

[18]  R. Hay,et al.  SUMO-1 modification of IkappaBalpha inhibits NF-kappaB activation. , 1998, Molecular cell.

[19]  E. Brignole,et al.  Disruption of PML Subnuclear Domains by the Acidic IE1 Protein of Human Cytomegalovirus Is Mediated through Interaction with PML and May Modulate a RING Finger-Dependent Cryptic Transactivator Function of PML , 1998, Molecular and Cellular Biology.

[20]  S. Weller,et al.  ND10 Protein PML Is Recruited to Herpes Simplex Virus Type 1 Prereplicative Sites and Replication Compartments in the Presence of Viral DNA Polymerase , 1998, Journal of Virology.

[21]  G. Hayward,et al.  Disruption of PML-associated nuclear bodies by IE1 correlates with efficient early stages of viral gene expression and DNA replication in human cytomegalovirus infection. , 2000, Virology.

[22]  R. Everett.  ICP0 Induces the Accumulation of Colocalizing Conjugated Ubiquitin , 2000, Journal of Virology.

[23]  M. Hochstrasser,et al.  A new protease required for cell-cycle progression in yeast , 1999, Nature.

[24]  S. Weller,et al.  Interactions of Herpes Simplex Virus Type 1 with ND10 and Recruitment of PML to Replication Compartments , 2001, Journal of Virology.

[25]  L. Frappier,et al.  The DNA segregation mechanism of Epstein–Barr virus nuclear antigen 1 , 2000, EMBO reports.

[26]  M. Ptashne,et al.  Chromatin components as part of a putative transcriptional repressing complex. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[27]  R. Everett,et al.  HSV‐1 IE protein Vmw110 causes redistribution of PML. , 1994, The EMBO journal.

[28]  R. Everett,et al.  The Ability of Herpes Simplex Virus Type 1 Immediate-Early Protein Vmw110 To Bind to a Ubiquitin-Specific Protease Contributes to Its Roles in the Activation of Gene Expression and Stimulation of Virus Replication , 1999, Journal of Virology.

[29]  R. Everett,et al.  A surprising role for the proteasome in the regulation of herpesvirus infection. , 1999, Trends in biochemical sciences.

[30]  A. Dejean,et al.  Targeting of adenovirus E1A and E4-ORF3 proteins to nuclear matrix- associated PML bodies , 1995, The Journal of cell biology.

[31]  W. Earnshaw,et al.  Specific destruction of kinetochore protein CENP‐C and disruption of cell division by herpes simplex virus immediate‐early protein Vmw110 , 1999, The EMBO journal.

[32]  C. Baumann,et al.  Non-apoptotic chromosome condensation induced by stress: delineation of interchromosomal spaces , 2000, Chromosoma.

[33]  P. Tegtmeyer,et al.  Replication but Not Transcription of Simian Virus 40 DNA Is Dependent on Nuclear Domain 10 , 2000, Journal of Virology.

[34]  W. O'brien,et al.  Interferon coordinately inhibits the disruption of PML-positive ND10 and immediate-early gene expression by herpes simplex virus. , 2000, Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.

[35]  R. Everett,et al.  The nuclear location of PML, a cellular member of the C3HC4 zinc-binding domain protein family, is rearranged during herpes simplex virus infection by the C3HC4 viral protein ICP0. , 1994, The Journal of general virology.

[36]  John Calvin Reed,et al.  Human Daxx regulates Fas‐induced apoptosis from nuclear PML oncogenic domains (PODs) , 1999, The EMBO journal.

[37]  Won-Jong Jang,et al.  Origin-Independent Assembly of Kaposi's Sarcoma-Associated Herpesvirus DNA Replication Compartments in Transient Cotransfection Assays and Association with the ORF-K8 Protein and Cellular PML , 2001, Journal of Virology.

[38]  L. Szekely,et al.  EBNA-5, an Epstein-Barr virus-encoded nuclear antigen, binds to the retinoblastoma and p53 proteins. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[39]  D. Lowy,et al.  The Papillomavirus Minor Capsid Protein, L2, Induces Localization of the Major Capsid Protein, L1, and the Viral Transcription/Replication Protein, E2, to PML Oncogenic Domains , 1998, Journal of Virology.

[40]  R. Everett,et al.  A viral activator of gene expression functions via the ubiquitin–proteasome pathway , 1998, The EMBO journal.

[41]  D. Spector,et al.  Visualization of gene activity in living cells , 2000, Nature Cell Biology.

[42]  J. Yewdell,et al.  Intracellular Localization of Proteasomal Degradation of a Viral Antigen , 1999, The Journal of cell biology.

[43]  E. Robertson,et al.  The latency-associated nuclear antigen tethers the Kaposi's sarcoma-associated herpesvirus genome to host chromosomes in body cavity-based lymphoma cells. , 1999, Virology.

[44]  G. Hayward,et al.  The Human Cytomegalovirus IE2 and UL112-113 Proteins Accumulate in Viral DNA Replication Compartments That Initiate from the Periphery of Promyelocytic Leukemia Protein-Associated Nuclear Bodies (PODs or ND10) , 1999, Journal of Virology.

[45]  P. Lieberman,et al.  Lytic but Not Latent Replication of Epstein-Barr Virus Is Associated with PML and Induces Sequential Release of Nuclear Domain 10 Proteins , 2000, Journal of Virology.

[46]  R. Everett.  ICP0, a regulator of herpes simplex virus during lytic and latent infection. , 2000, BioEssays : news and reviews in molecular, cellular and developmental biology.

[47]  T. Sternsdorf,et al.  The Nuclear Dot Protein Sp100, Characterization of Domains Necessary for Dimerization, Subcellular Localization, and Modification by Small Ubiquitin-like Modifiers* , 1999, The Journal of Biological Chemistry.

[48]  G. Maul,et al.  Human Cytomegalovirus Immediate Early Interaction with Host Nuclear Structures: Definition of an Immediate Transcript Environment , 1997, The Journal of cell biology.

[49]  R. Everett,et al.  Alphaherpesvirus Proteins Related to Herpes Simplex Virus Type 1 ICP0 Induce the Formation of Colocalizing, Conjugated Ubiquitin , 2001, Journal of Virology.

[50]  B. Plachter,et al.  The nuclear domain 10 (ND10) is disrupted by the human cytomegalovirus gene product IE1. , 1996, Experimental cell research.

[51]  M. Botchan,et al.  Segregation of viral plasmids depends on tethering to chromosomes and is regulated by phosphorylation. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[52]  G. Maul.  Nuclear domain 10, the site of DNA virus transcription and replication , 1998, BioEssays : news and reviews in molecular, cellular and developmental biology.

[53]  G. Shaw,et al.  Human Papillomavirus DNA Replication Compartments in a Transient DNA Replication System , 1999, Journal of Virology.

[54]  A. Dejean,et al.  Interaction of SP100 with HP1 proteins: a link between the promyelocytic leukemia-associated nuclear bodies and the chromatin compartment. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[55]  Jennifer O'Neil,et al.  Sequestration and Inhibition of Daxx-Mediated Transcriptional Repression by PML , 2000, Molecular and Cellular Biology.

[56]  R. Everett,et al.  Herpes Simplex Virus Type 1 Immediate-Early Protein Vmw110 Induces the Proteasome-Dependent Degradation of the Catalytic Subunit of DNA-Dependent Protein Kinase , 1999, Journal of Virology.

[57]  R. Everett,et al.  The adenovirus type 5 E1b 55K and E4 Orf3 proteins associate in infected cells and affect ND10 components. , 1999, The Journal of general virology.

[58]  R. Everett.  Functional and genetic analysis of the role of Vmw110 in herpes simplex virus replication , 1991 .

[59]  L. Szekely,et al.  Proteins associated with the promyelocytic leukemia gene product (PML)-containing nuclear body move to the nucleolus upon inhibition of proteasome-dependent protein degradation. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[60]  M. Weitzman,et al.  Adenovirus replication is coupled with the dynamic properties of the PML nuclear structure. , 1996, Genes & development.

[61]  R. Everett,et al.  Human Neuron-Committed Teratocarcinoma NT2 Cell Line Has Abnormal ND10 Structures and Is Poorly Infected by Herpes Simplex Virus Type 1 , 2001, Journal of Virology.

[62]  S. Kenney,et al.  Epstein-Barr Virus Immediate-Early Protein BZLF1 Is SUMO-1 Modified and Disrupts Promyelocytic Leukemia Bodies , 2001, Journal of Virology.

[63]  G. Hayward,et al.  Evaluation of Interactions of Human Cytomegalovirus Immediate-Early IE2 Regulatory Protein with Small Ubiquitin-Like Modifiers and Their Conjugation Enzyme Ubc9 , 2001, Journal of Virology.

[64]  G. Wilkinson,et al.  Disruption of PML-associated nuclear bodies mediated by the human cytomegalovirus major immediate early gene product. , 1998, The Journal of general virology.

[65]  P. Freemont.  Ubiquitination: RING for destruction? , 2000, Current Biology.

[66]  R. Everett,et al.  Herpes Simplex Virus Type 1 Immediate-Early Protein Vmw110 Inhibits Progression of Cells through Mitosis and from G1 into S Phase of the Cell Cycle , 1999, Journal of Virology.

[67]  C. Preston.  Repression of viral transcription during herpes simplex virus latency. , 2000, The Journal of general virology.

[68]  Mounira K Chelbi-Alix,et al.  Herpes virus induced proteasome-dependent degradation of the nuclear bodies-associated PML and Sp100 proteins , 1999, Oncogene.

[69]  L. Szekely,et al.  Intranuclear redistribution of SV40T, p53, and PML in a conditionally SV40T-immortalized cell line. , 1996, Experimental cell research.

[70]  G. Maul,et al.  Modification of discrete nuclear domains induced by herpes simplex virus type 1 immediate early gene 1 product (ICP0). , 1993, The Journal of general virology.

[71]  G. G. Stokes.  "J." , 1890, The New Yale Book of Quotations.

[72]  K. Mossman,et al.  Herpes Simplex Virus ICP0 Mutants Are Hypersensitive to Interferon , 2000, Journal of Virology.

[73]  Paul Freemont,et al.  Role of Promyelocytic Leukemia (Pml) Sumolation in Nuclear Body Formation, 11s Proteasome Recruitment, and as2O3-Induced Pml or Pml/Retinoic Acid Receptor α Degradation , 2001, The Journal of experimental medicine.

[74]  R. van Driel,et al.  Cell cycle regulation of PML modification and ND10 composition. , 1999, Journal of cell science.

[75]  P. Lambert,et al.  Interaction of the papillomavirus transcription/replication factor, E2, and the viral capsid protein, L2. , 2000, Virology.

[76]  D. Brough,et al.  Efficient Activation of Viral Genomes by Levels of Herpes Simplex Virus ICP0 Insufficient To Affect Cellular Gene Expression or Cell Survival , 2001, Journal of Virology.