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Journal of Virology, December 2007, p. 12836-12845, Vol. 81, No. 23
0022-538X/07/$08.00+0     doi:10.1128/JVI.01804-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Kaposi's Sarcoma-Associated Herpesvirus Encodes an Ortholog of miR-155{triangledown} ,{dagger}

Rebecca L. Skalsky, Mark A. Samols, Karlie B. Plaisance, Isaac W. Boss, Alberto Riva, M. Cecilia Lopez, Henry V. Baker, and Rolf Renne*

Department of Molecular Genetics and Microbiology, and Shands Cancer Center, University of Florida, Gainesville, Florida

Received 16 August 2007/ Accepted 11 September 2007

MicroRNAs (miRNAs) are small noncoding RNAs that posttranscriptionally regulate gene expression by binding to 3'-untranslated regions (3'UTRs) of target mRNAs. Kaposi's sarcoma-associated herpesvirus (KSHV), a virus linked to malignancies including primary effusion lymphoma (PEL), encodes 12 miRNA genes, but only a few regulatory targets are known. We found that KSHV-miR-K12-11 shares 100% seed sequence homology with hsa-miR-155, an miRNA frequently found to be up-regulated in lymphomas and critically important for B-cell development. Based on this seed sequence homology, we hypothesized that both miRNAs regulate a common set of target genes and, as a result, could have similar biological activities. Examination of five PEL lines showed that PELs do not express miR-155 but do express high levels of miR-K12-11. Bioinformatic tools predicted the transcriptional repressor BACH-1 to be targeted by both miRNAs, and ectopic expression of either miR-155 or miR-K12-11 inhibited a BACH-1 3'UTR-containing reporter. Furthermore, BACH-1 protein levels are low in cells expressing either miRNA. Gene expression profiling of miRNA-expressing stable cell lines revealed 66 genes that were commonly down-regulated. For select genes, miRNA targeting was confirmed by reporter assays. Thus, based on our in silico predictions, reporter assays, and expression profiling data, miR-K12-11 and miR-155 regulate a common set of cellular targets. Given the role of miR-155 during B-cell maturation, we speculate that miR-K12-11 may contribute to the distinct developmental phenotype of PEL cells, which are blocked in a late stage of B-cell development. Together, these findings indicate that KSHV miR-K12-11 is an ortholog of miR-155.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, and Shands Cancer Center, 1376 Mowry Road, Gainesville, FL 32610-3633. Phone: (352) 273-8204. Fax: (352) 273-8299. E-mail: rrenne{at}ufl.edu

{triangledown} Published ahead of print on 19 September 2007.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, December 2007, p. 12836-12845, Vol. 81, No. 23
0022-538X/07/$08.00+0     doi:10.1128/JVI.01804-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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