Lessons from the Pros

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Science  19 Jun 2009:
Vol. 324, Issue 5934, pp. 1493
DOI: 10.1126/science.324_1493c

Human cells contain tens of thousands of protein-encoding genes that are transcribed into a much larger numbers of mRNAs. Viruses, on the other hand, are far simpler, carrying with them only a handful of genes and proteins, yet they have developed countless ways of hijacking specific host cellular functions for their own benefit. Discovering these survival mechanisms often offers fascinating insights into normal host cell biology. Eukaryotes use sophisticated ways of regulating gene expression, including polyadenylating the 3′ end of mRNAs to enhance their stability for eventual translation into protein, and possibly also to promote mRNA degradation. Some herpesviruses, including Kaposi's sarcoma–associated herpesvirus (KSHV), manipulate host cells by promoting the widespread destruction of cellular mRNAs. KSHV achieves this via its Sox protein, and Lee and Glaunsinger show that human cells expressing the viral Sox protein contain mRNAs with unusually long poly(A) tails (hyperadenylation), which was mediated by the host enzyme poly(A) polymerase II. This effect of viral Sox was linked to its ability to accelerate mRNA turnover, suggesting that the virus induces host mRNA degradation by modulating poly(A) length.

PLoS Biol. 7, e1000107 (2009).

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