Published in: J. Gen. Virol. vol. 83, no. 1, pp. 179-188 (January, 2002):
"Latent Nuclear Antigen of Kaposi's Sarcoma Herpesvirus/Human Herpesvirus-8 Induces and Relocates RING3 to Nuclear Heterochromatin Regions."

Mattsson K,  Kiss C,  Platt GM,  Simpson GR,  Kashuba E,  Klein G,  Schulz TF,  and Szekely L.

Microbiology and Tumor Biology Center, Karolinska Institute, PO Box 280, S-171 77, Stockholm, Sweden Department of Virology, Hannover Medical School, D-30623 Hannover, Germany
Molecular Virology Group, Department of Medical Microbiology, The University of Liverpool, Liverpool, UK.



Abstract:

LANA, the major latency-associated nuclear antigen of Kaposi's sarcoma herpesvirus/human herpesvirus-8 (KSHV/HHV-8), binds RING3 protein, one of five human homologues of the fsh (female sterile homeotic) gene product of DROSOPHILA: In KSHV/HHV-8-infected cells LANA and the viral episomes accumulate
in heterochromatin-associated nuclear bodies. Here we show that in several KSHV/HHV-8-negative cell lines derived from carcinomas, sarcomas and lymphomas, RING3 was expressed at low levels, primarily localized to the euchromatin, and dissociated from the chromosomes during mitosis. In contrast, in KSHV/HHV-8-infected body cavity lymphoma cells the bulk of RING3 localizes to the LANA nuclear bodies and remains associated with the chromosomes during cell division. KSHV/HHV-8-infected body cavity lymphoma cells expressed RING3 at much higher levels than cells without the virus. Transfection of full-length LANA, but not the C terminus alone, greatly induced RING3 gene expression, and LANA and RING3 co-localized even in the transfected cells, in the absence of KSHV/HHV-8 viral DNA. High levels of LANA expression led to the disappearance of heterochromatin in both human and mouse cells. We suggest that LANA and RING3 may create a local euchromatic microenvironment around the viral episomes that are anchored to the heterochromatin.



Additional References:

1. Maruo S, Nanbo A, and Takada K, "Replacement of the Epstein-Barr Virus Plasmid with the EBER Plasmid in Burkitt's Lymphoma Cells", J. Virology, vol. 75, no. 20, pp. 9977-9982 (October, 2001).

2.  Takada K, and Nanbo A, "The Role of EBERs in Oncogenesis", Seminars in Cancer Biology, vol. 11, no. 6, pp. 461-467 (December, 2001).

3. Vinogradova T, Leppik L, Kalinina E, Zhilidov P, Grzeschik K-H, and Sverdlov E, "Selective Differential Display of RNAs Containing Interspersed Repeats: Analysis of Changes in the Transcription of HERV-K LTRs in Germ Cell Tumors", Molecular Genetics and Genomics vol. 266, no. 5, pp. 796 805 (January, 2002).

4. Frenster JH, "Activation of  DNA Transcription within Repressed Chromatin", 14th John Innes Symposium, September 5-8,  2001.

5. Eddy SR, "Non-Coding RNA Genes and the  Modern RNA World", Nature Reviews Genetics, vol. 2, no. 12, pp. 919-929 (December, 2001).

6. Frenster JH, "Oncogenes as Molecular Targets within Active Chromatin", Clinical Cancer Research, vol. 5, suppl. l, p. 3855s, (624), (November, 1999):



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euchromatin:  "the most active portion of the genome within the cell nucleus".