Annexation of the interchromosomal space during viral infection

Monier, Karine; Armas, Juan Carlos González; Etteldorf, Susanne; Ghazal, Peter; Sullivan, Kevin F.

doi:10.1038/35023615

Cited by 149 publications

(165 citation statements)

References 27 publications

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“…1v and ix). These findings were similar to those reported previously (18,26). Mock-infected cells showed no significant ICP8 staining (Fig.…”

Section: Vol 78 2004 Late Maturation Of Hsv-1 Replication Compartmesupporting

confidence: 83%

“…During RC formation and annexation of space in the host cell nucleus, cellular chromatin is marginalized and compressed (18,26). This results in a layer of host cell chromatin surrounding the RC, which potentially constitutes a barrier through which viral capsids must move to reach the INM.…”

mentioning

confidence: 99%

“…Herpesvirus particles are then thought to fuse with the outer nuclear membrane, releasing viral nucleocapsids into the host cell cytosol (17, 28). Finally, the nucleocapsid undergoes secondary envelopment and egress from the cell (24).During RC formation and annexation of space in the host cell nucleus, cellular chromatin is marginalized and compressed (18,26). This results in a layer of host cell chromatin surrounding the RC, which potentially constitutes a barrier through which viral capsids must move to reach the INM.…”

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confidence: 99%

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Herpes Simplex Virus 1 U _L 31 and U _L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Simpson-Holley

Baines

Roller

et al. 2004

J Virol

121

127

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Herpes simplex virus 1 (HSV-1) forms replication compartments (RCs), domains in which viral DNA replication, late-gene transcription, and encapsidation take place, in the host cell nucleus. The formation of these domains leads to compression and marginalization of host cell chromatin, which forms a dense layer surrounding the viral RCs and constitutes a potential barrier to viral nuclear egress or primary envelopment at the inner nuclear membrane. Surrounding the chromatin layer is the nuclear lamina, a further host cell barrier to egress. In this study, we describe an additional phase in RC maturation that involves disruption of the host chromatin and nuclear lamina so that the RC can approach the nuclear envelope. During this phase, the structure of the chromatin layer is altered so that it no longer forms a continuous layer around the RCs but instead is fragmented, forming islands between which RCs extend to reach the nuclear periphery. Coincident with these changes, the nuclear lamina components lamin A/C and lamin-associated protein 2 appear to be redistributed via a mechanism involving the U L 31 and U L 34 gene products. Viruses in which the U L 31 or U L 34 gene has been deleted are unable to undergo this phase of chromatin reorganization and lamina alterations and instead form RCs which are bounded by an intact host cell chromatin layer and nuclear lamina. We postulate that these defects in chromatin restructuring and lamina reorganization explain the previously documented growth defects of these mutant viruses.Herpes simplex virus 1 (HSV-1) is a large double-stranded DNA virus which replicates in the nucleus of infected host cells. Viral DNA replication and late gene transcription occur in replication compartments (RCs), nuclear domains which are formed when viral replication successively annexes large portions of the nucleus during the early stages of infection. During the later stages of replication, assembly of viral capsids occurs and DNA packaging takes place in RCs. Following this, capsids move to the inner nuclear membrane (INM), where primary envelopment takes place as they bud into the perinuclear space, acquiring an envelope derived from the INM. Herpesvirus particles are then thought to fuse with the outer nuclear membrane, releasing viral nucleocapsids into the host cell cytosol (17, 28). Finally, the nucleocapsid undergoes secondary envelopment and egress from the cell (24).During RC formation and annexation of space in the host cell nucleus, cellular chromatin is marginalized and compressed (18,26). This results in a layer of host cell chromatin surrounding the RC, which potentially constitutes a barrier through which viral capsids must move to reach the INM. Thus, to bud through the INM, viral nucleocapsids must move through the compacted host chromatin and the nuclear lamina. The nuclear lamina, a proteinaceous layer underlying the INM, is composed of integral INM proteins such as lamin-associated protein 2 (LAP2) and lamin B receptor, which interact with lamin proteins A, B, and C (2, ...

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“…1v and ix). These findings were similar to those reported previously (18,26). Mock-infected cells showed no significant ICP8 staining (Fig.…”

Section: Vol 78 2004 Late Maturation Of Hsv-1 Replication Compartmesupporting

confidence: 83%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Herpes Simplex Virus 1 U _L 31 and U _L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Simpson-Holley

Baines

Roller

et al. 2004

J Virol

121

127

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“…Then, we asked whether these ori-Lytassociated cellular proteins are recruited to VRCs during the DNA replication. VRCs are intranuclear domains which are formed when viral replication successively annexes a large portion of the nucleus and the location where viral DNA replication takes place in the host cell nucleus (29). In herpesviruses, VRCs are visible in IFAs as large, irregularly shaped nuclear domains.…”

Section: Resultsmentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus ori - Lyt -Dependent DNA Replication: Involvement of Host Cellular Factors

Wang

Tang

et al. 2008

J Virol

111

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Herpesvirus lytic DNA replication requires both the cis-acting element, the origin, and trans-acting factors, including virally encoded origin-binding protein, DNA replication enzymes, and auxiliary factors. Two lytic DNA replication origins (ori-Lyt) of Kaposi's sarcoma-associated herpesvirus (KSHV) have been identified, and two virally encoded proteins, namely, RTA and K8, have been shown to bind to the origins. In this study, we sought to identify cellular factors that associate with ori-Lyt by using DNA affinity purification and mass spectrometry. This approach led to identification of several cellular proteins that bind to KSHV ori-Lyt. They include topoisomerases (Topo) I and II, MSH2/6, RecQL, poly(ADP-ribose) polymerase I (PARP-1), DNA-PK, Ku86/70 autoantigens, and scaffold attachment factor A (SAF-A). RecQL appears to associate with prereplication complexes and be recruited to ori-Lyt through RTA and K8. Topoisomerases, MSH2, PARP-1, DNA-PK, and Ku86 were not detected in prereplication complexes but were present in replication initiation complexes on ori-Lyt. All these cellular proteins accumulate in viral replication compartments in the nucleus, indicating that these proteins may have a role in viral replication. Topo I and II appear to be essential for viral DNA replication as inhibition of their activities with specific inhibitors (camptothecin and ellipticine) blocked ori-Lyt-dependent DNA replication. Furthermore, inhibition of PARP-1 with chemical inhibitors (3-aminobenzamide and niacinamide) resulted in decreased ori-Lyt-dependent DNA replication, whereas hydroxyurea, which raises PARP-1 activity, caused an increase in the DNA replication, suggesting a positive role for PARP-1 in KSHV lytic DNA replication.Kaposi's sarcoma-associated herpesvirus (KSHV), also referred to as human herpesvirus 8, is the etiologic agent of several AIDS-associated malignancies, including Kaposi's sarcoma (KS), primary effusion lymphoma, and multicentric Castleman's disease (1,17,33). In KS lesions, most spindle cells of endothelial origin are latently infected with KSHV, and a small percentage of these cells undergo spontaneous lytic replication (34,35,43). Increasing evidence suggests that the small percentage of cells experiencing viral lytic replication play important roles in viral pathogenicity. Treatment of KS patients or AIDS patients at risk for KS with antiherpesviral drugs, like foscarnet and ganciclovir, which are known to block lytic DNA replication, results in regression of KS lesions or a decease in the incidence of KS development. The lytic replication cycle directly contributes to viral tumorigenesis by spreading viruses to target cells and by providing paracrine regulation for KS development (11). A recent study by Grundhoff and Ganem (19) suggests a new role for lytic replication in sustaining the population of latently infected cells that otherwise would be quickly lost by segregation of latent viral episomes as spindle cells divide. Thus, unlike with other oncogenic viruses, where the latent life c...

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“…Chromosomes reside in a specific territory of 1.8% -12% of the nuclear volume (human HT-1080 cells [Müller et al 2010]). The nuclear volume estimate for yeast is from Jorgensen et al (2007) and for human HeLa cells from Monier et al (2000). tion complexes.…”

Section: Transcribed Genementioning

confidence: 99%

Regulation of Recombination and Genomic Maintenance

Heyer

2015

Cold Spring Harb Perspect Biol

104

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Recombination is a central process to stably maintain and transmit a genome through somatic cell divisions and to new generations. Hence, recombination needs to be coordinated with other events occurring on the DNA template, such as DNA replication, transcription, and the specialized chromosomal functions at centromeres and telomeres. Moreover, regulation with respect to the cell-cycle stage is required as much as spatiotemporal coordination within the nuclear volume. These regulatory mechanisms impinge on the DNA substrate through modifications of the chromatin and directly on recombination proteins through a myriad of posttranslational modifications (PTMs) and additional mechanisms. Although recombination is primarily appreciated to maintain genomic stability, the process also contributes to gross chromosomal arrangements and copy-number changes. Hence, the recombination process itself requires quality control to ensure high fidelity and avoid genomic instability. Evidently, recombination and its regulatory processes have significant impact on human disease, specifically cancer and, possibly, neurodegenerative diseases.

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Annexation of the interchromosomal space during viral infection

Cited by 149 publications

References 27 publications

Herpes Simplex Virus 1 U _L 31 and U _L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Herpes Simplex Virus 1 U _L 31 and U _L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Kaposi's Sarcoma-Associated Herpesvirus ori - Lyt -Dependent DNA Replication: Involvement of Host Cellular Factors

Regulation of Recombination and Genomic Maintenance

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Annexation of the interchromosomal space during viral infection

Cited by 149 publications

References 27 publications

Herpes Simplex Virus 1 U L 31 and U L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Herpes Simplex Virus 1 U L 31 and U L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Kaposi's Sarcoma-Associated Herpesvirus ori - Lyt -Dependent DNA Replication: Involvement of Host Cellular Factors

Regulation of Recombination and Genomic Maintenance

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Product

Resources

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Herpes Simplex Virus 1 U _L 31 and U _L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery

Herpes Simplex Virus 1 U _L 31 and U _L 34 Gene Products Promote the Late Maturation of Viral Replication Compartments to the Nuclear Periphery