Virus-mediated mRNA decay by hyperadenylation 英文参考文献.docVIP

Minireview Virus-mediated mRNA decay by hyperadenylation Kevin J Sokoloski, Emily L Chaskey and Jeffrey Wilusz Address: Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. Correspondence: Jeffrey Wilusz. Email: jeffrey.wilusz@ little to guide them as they set out to define the mechanism of SOX-induced RNA decay. Abstract Degradation of cellular mRNAs during Kaposi’s sarcoma-asso- ciated herpesvirus infection is associated with hyperadenylation of transcripts and a relocalization of cytoplasmic poly(A)-binding proteins to the nucleus. Through a careful analysis of mRNA modifications, locali- zation, and RNA-binding proteins during SOX-induced mRNA degradation, Lee and Glaunsinger made four key observations using a series of transfections and viral infections in human 293T and TIME (telomerase-immor- The cellular machinery for RNA decay plays a major role in regulating gene expression and as a mechanism for RNA quality control [1]. Increasing evidence suggests that viruses have evolved ways of interfacing with the cellular RNA decay machinery that aid their survival and replica- tion. First, viral transcripts must avoid degradation if they are to be effectively translated. Second, viruses often induce the degradation of cellular mRNAs, which gives their own transcripts a competitive edge for access to the cellular translation machinery. The mechanisms under- lying these strategies are currently being elucidated. In addition to providing a clearer understanding of virus-host interactions, the mechanisms used by viruses to usurp the cellular RNA decay machinery may also provide insight talized microvascular endothelial) cells. First, they documented a clear increase in the size of the poly(A) tail of target RNAs in the presence of SOX that cor