MAREKS-DISEASE VIRUS LATENCY-ASSOCIATED TRANSCRIPTS BELONG TO A FAMILY OF SPLICED RNAS THAT ARE ANTISENSE TO THE ICP4 HOMOLOG GENE

Citation
Jl. Cantello et al., MAREKS-DISEASE VIRUS LATENCY-ASSOCIATED TRANSCRIPTS BELONG TO A FAMILY OF SPLICED RNAS THAT ARE ANTISENSE TO THE ICP4 HOMOLOG GENE, Journal of virology, 71(2), 1997, pp. 1353-1361
Citations number
39
Categorie Soggetti
Virology
Journal title
ISSN journal
0022538X
Volume
71
Issue
2
Year of publication
1997
Pages
1353 - 1361
Database
ISI
SICI code
0022-538X(1997)71:2<1353:MVLTBT>2.0.ZU;2-8
Abstract
Marek's disease virus (MDV) latency-associated transcripts include at least two MDV small RNAs (MSRs) and a 10-kb RNA which map antisense to the ICP4 homolog gene and are relatively abundant in MDV-transformed lymphoblastoid cells. This report further describes the biological and structural properties of these RNAs. First, these RNAs were detected in primary lymphomas isolated from chickens infected with several onco genic MDV strains. Second, the MSRs are nonpolyadenylated, whereas, th e 10-kb RNA is predominantly polyadenylated. Third, MSRs localize to t he nuclei of both lymphoblastoid cells and cytolytically infected chic ken embryo fibroblasts. Fourth, the 3'-region splice junctions of the MSRs during latent and productive infection were determined by sequenc ing RNA-PCR products generated with primers that flank the 3' splice r egion. The MSRs contain at least three introns, the largest of which o verlaps the ICP4 putative translational start site. Fifth, the 5' end of the MSRs initiates approximately 5 kb upstream from the main body o f the RNA. The extreme 5' exon is approximately 251 nucleotides (nt) l ong and is joined to the main body of the transcript upon removal of a 4,852-nt intron. Finally, the 10-kb RNA lies entirely within the repe ats Banking the unique short region of the genome. We believe that the MSRs and 10-kb RNA belong to a family of spliced RNAs that map antise nse to the ICP4 gene and comprise a complex transcriptional unit expre ssed during MDV-induced T-cell transformation.