UNIGE document Scientific Article
previous document  unige:38137  next document
add to browser collection

Sendai virus trailer RNA binds TIAR, a cellular protein involved in virus-induced apoptosis

Kedersha, Nancy
Anderson, Paul
Published in EMBO journal. 2002, vol. 21, no. 19, p. 5141-50
Abstract Sendai virus (SeV) leader (le) and trailer (tr) RNAs are short transcripts generated during abortive antigenome and genome synthesis, respectively. Recom binant SeV (rSeV) that express tr-like RNAs from the leader region are non-cytopathic and, moreover, prevent wild-type SeV from inducing apoptosis in mixed infections. These rSeV thus appear to have gained a function. Here we report that tr RNA binds to a cellular protein with many links to apoptosis (TIAR) via the AU-rich sequence 5' UUUUAAAUUUU. Duplication of this AU-rich sequence alone within the le RNA confers TIAR binding on this le* RNA and a non-cytopathic phenotype to these rSeV in cell culture. Transgenic overexpression of TIAR during SeV infection promotes apoptosis and reverses the anti-apoptotic effects of le* RNA expression. More over, TIAR overexpression and SeV infection act synergistically to induce apoptosis. These short viral RNAs may act by sequestering TIAR, a multivalent RNA recognition motif (RRM) family RNA-binding protein involved in SeV-induced apoptosis. In this view, tr RNA is not simply a by-product of abortive genome synthesis, but is also an antigenome transcript that modulates the cellular antiviral response.
Keywords Apoptosis/physiologyCloning, MolecularCytoplasm/metabolismDNA DamageHeLa CellsHumansPromoter Regions, GeneticRNA, Viral/geneticsRNA-Binding Proteins/metabolismRespirovirus Infections/virologySendai virus/genetics/pathogenicityTranscription, Genetic
PMID: 12356730
Full text
Article (Published version) (325 Kb) - public document Free access
Research group Virologie moléculaire (275)
(ISO format)
ISENI, Frédéric et al. Sendai virus trailer RNA binds TIAR, a cellular protein involved in virus-induced apoptosis. In: EMBO journal, 2002, vol. 21, n° 19, p. 5141-50. doi: 10.1093/emboj/cdf513 https://archive-ouverte.unige.ch/unige:38137

510 hits



Deposited on : 2014-06-25

Export document
Format :
Citation style :