Abstract
HSV regulatory proteins ICP0 and VP16 independently regulate transcription of the ICP0 gene during virus infection. In this study, we tried to determine the possible regulatory mechanism of ICP0 expression during virus infection. Among eight putative VP16 binding sites present in the ICP0 regulatory sequence, the most upstream one alone was sufficiently responsive to VP16-mediated activation. When the G/C-rich sequence present in front of the last TAATGARAT sequence of the ICP0 promoter was either deleted or point mutated, the activational effect of VP16 on the promoter was completely abolished. Furthermore, according to the gel mobility shift assay using a labeled double-stranded oligonucleotide derived from the G/C-rich sequence in the ICP0 promoter, specific protein binding to the probe was clearly demonstrated and was approximately fivefold upregulated by HSV-1 infection. Therefore, the G/C-rich sequence might play a critical role in VP16-mediated activation of the ICP0 promoter and the effect may be a result of the enhanced binding of a protein to the G/C-rich sequence during virus infection. (C) 2000 Academic Press.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 15-19 |
| Number of pages | 5 |
| Journal | Molecular Cell Biology Research Communications |
| Volume | 3 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 1 2000 |
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All Science Journal Classification (ASJC) codes
- Molecular Biology
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Transcriptional regulation of herpes simplex virus type 1 ICP0 promoter by virion protein 16. / Kwun, Hyun Jin; Jang, Kyung Lib.
In: Molecular Cell Biology Research Communications, Vol. 3, No. 1, 01.01.2000, p. 15-19.Research output: Contribution to journal › Article
TY - JOUR
T1 - Transcriptional regulation of herpes simplex virus type 1 ICP0 promoter by virion protein 16
AU - Kwun, Hyun Jin
AU - Jang, Kyung Lib
PY - 2000/1/1
Y1 - 2000/1/1
N2 - HSV regulatory proteins ICP0 and VP16 independently regulate transcription of the ICP0 gene during virus infection. In this study, we tried to determine the possible regulatory mechanism of ICP0 expression during virus infection. Among eight putative VP16 binding sites present in the ICP0 regulatory sequence, the most upstream one alone was sufficiently responsive to VP16-mediated activation. When the G/C-rich sequence present in front of the last TAATGARAT sequence of the ICP0 promoter was either deleted or point mutated, the activational effect of VP16 on the promoter was completely abolished. Furthermore, according to the gel mobility shift assay using a labeled double-stranded oligonucleotide derived from the G/C-rich sequence in the ICP0 promoter, specific protein binding to the probe was clearly demonstrated and was approximately fivefold upregulated by HSV-1 infection. Therefore, the G/C-rich sequence might play a critical role in VP16-mediated activation of the ICP0 promoter and the effect may be a result of the enhanced binding of a protein to the G/C-rich sequence during virus infection. (C) 2000 Academic Press.
AB - HSV regulatory proteins ICP0 and VP16 independently regulate transcription of the ICP0 gene during virus infection. In this study, we tried to determine the possible regulatory mechanism of ICP0 expression during virus infection. Among eight putative VP16 binding sites present in the ICP0 regulatory sequence, the most upstream one alone was sufficiently responsive to VP16-mediated activation. When the G/C-rich sequence present in front of the last TAATGARAT sequence of the ICP0 promoter was either deleted or point mutated, the activational effect of VP16 on the promoter was completely abolished. Furthermore, according to the gel mobility shift assay using a labeled double-stranded oligonucleotide derived from the G/C-rich sequence in the ICP0 promoter, specific protein binding to the probe was clearly demonstrated and was approximately fivefold upregulated by HSV-1 infection. Therefore, the G/C-rich sequence might play a critical role in VP16-mediated activation of the ICP0 promoter and the effect may be a result of the enhanced binding of a protein to the G/C-rich sequence during virus infection. (C) 2000 Academic Press.
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U2 - 10.1006/mcbr.2000.0179
DO - 10.1006/mcbr.2000.0179
M3 - Article
VL - 3
SP - 15
EP - 19
JO - Molecular Cell Biology Research Communications
JF - Molecular Cell Biology Research Communications
SN - 1522-4724
IS - 1
ER -