Increased levels of B1 and B2 SINE transcripts in mouse fibroblast cells due to minute virus of mice infection.
Minute virus of mice (MVM), an autonomous parvovirus, has served as a model for understanding parvovirus infection including host cell response to infection. In this paper, we report the effect of MVM infection on host cell gene expression in mouse fibroblast cells (LA9 cells), analyzed by differential display. Somewhat surprisingly, our data reveal that few cellular protein-coding genes appear to be up- or downregulated and identify the murine B1 and B2 short interspersed element (SINE) transcripts as being increased upon MVM infection. Primer extension assays confirm the effect of MVM infection on SINE expression and demonstrate that both SINEs are upregulated in a roughly linear fashion throughout MVM infection. They also demonstrate that the SINE response was due to RNA polymerase III transcription and not contaminating DNA or RNA polymerase II transcription. Furthermore, expression of MVM NS1, the major nonstructural protein, by transient transfection also leads to an increase in both murine SINEs. We believe this is the first time that the B1 and B2 SINEs have been shown to be altered by viral infection and the first time parvovirus infection has been shown to increase SINE expression. The increase in SINE transcripts caused by MVM infection does not appear to be due to an increase in either of the basal transcription factors TFIIIC110 or 220, in contrast to that which has been shown for other viruses.
Williams
Warren P
WP
Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.
Tamburic
Lillian
L
Astell
Caroline R
CR
D000818:Animals; D002460:Cell Line; D005347:Fibroblasts / Q000821:virology*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D051379:Mice; D008915:Minute Virus of Mice / Q000235:genetics / Q000472:pathogenicity*; D020086:Short Interspersed Nucleotide Elements / Q000235:genetics / Q000502:physiology*; D014158:Transcription, Genetic; D015854:Up-Regulation