The stable 2-kilobase latency-associated transcript of herpes simplex virus type 1 can alter the assembly of the 60S ribosomal subunit and is exported from nucleus to cytoplasm by a CRM1-dependent pathway.
During latency of herpes simplex virus type 1 in the neurons of the peripheral nervous system, the major transcript detected is the 2-kb latency-associated transcript (LAT) intron. During lytic infection, this intron has been shown to associate with ribosomes, suggesting a role in modifying the translational machinery of infected cells. In this study we show, using LAT-transfected cells, that the interaction of the intron with the 60S ribosomal subunit leads to irreversible changes in the sedimentation profile of this subunit in the nucleus. Furthermore, the 2-kb LAT intron is transported to the cytoplasm as part of the 60S ribosomal subunit, using a CRM1-dependent pathway.
Atanasiu
Doina
D
Department of Microbiology, University of Pennsylvania School of Medicine, 3610 Hamilton Walk, Philadelphia, PA 19104, USA.
Fraser
Nigel W
NW
D001692:Biological Transport; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism*; D018259:Herpesvirus 1, Human / Q000235:genetics*; D006801:Humans; D007438:Introns; D028884:Karyopherins / Q000502:physiology*; D012333:RNA, Messenger / Q000235:genetics*; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology*; D012270:Ribosomes / Q000378:metabolism*; D000097606:Exportin 1 Protein
D028884:Karyopherins; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D000097606:Exportin 1 Protein