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Nucleic Acids Research Advance Access originally published online on September 3, 2009
Nucleic Acids Research 2009 37(19):6515-6527; doi:10.1093/nar/gkp633
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Nucleic Acids Research, 2009, Vol. 37, No. 19 6515-6527
© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

Herpesvirus protein ICP27 switches PML isoform by altering mRNA splicing

Takayuki Nojima1,2, Takako Oshiro-Ideue1, Hiroto Nakanoya1, Hidenobu Kawamura1, Tomomi Morimoto3, Yasushi Kawaguchi3, Naoyuki Kataoka4 and Masatoshi Hagiwara1,2,*

1Laboratory of Gene Expression, School of Biomedical Science, 2Department of Functional Genomics, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8510, 3Department of Infectious Disease Control, International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Shirokanedai 4-6-1, Minato-ku, Tokyo 108-8639, Japan and 4Medical Top Track (MTT) Program, Medical Research Institute, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8510

*To whom correspondence should be addressed. Tel: +81 3 5803 5836; Fax: +81 3 5803 5853; Email: m.hagiwara.end{at}mri.tmd.ac.jp

Received April 30, 2009. Revised July 6, 2009. Accepted July 16, 2009.

Viruses use alternative splicing to produce a broad series of proteins from small genomes by utilizing the cellular splicing machinery. Since viruses use cellular RNA binding proteins for viral RNA processing, it is presumable that the splicing of cellular pre-mRNAs is affected by viral infection. Here, we showed that herpes simplex virus type 2 (HSV-2) modifies the expression of promyelocytic leukemia (PML) isoforms by altering pre-mRNA splicing. Using a newly developed virus-sensitive splicing reporter, we identified the viral protein ICP27 as an alternative splicing regulator of PML isoforms. ICP27 was found to bind preferentially to PML pre-mRNA and directly inhibit the removal of PML intron 7a in vitro. Moreover, we demonstrated that ICP27 functions as a splicing silencer at the 3' splice site of the PML intron 7a. The switching of PML isoform from PML-II to PML-V as induced by ICP27 affected HSV-2 replication, suggesting that the viral protein modulates the splicing code of cellular pre-mRNA(s) governing virus propagation.


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