Role of the cellular transcription factor YY1 in the latent-lytic switch of Kaposi's sarcoma-associated herpesvirus

Abstract Lytic cycle reactivation of Kaposi's sarcoma-associated herpesvirus (KSHV) is initiated by expression of the ORF50 gene. Here we show that YY1 protein specifically binds to the ORF50 promoter (ORF50p) region in vitro and in vivo . After treatment with chemical inducers, including sodiu...

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Published inVirology (New York, N.Y.) Vol. 413; no. 2; pp. 194 - 204
Main Authors Chang, Pey-Jium, Chen, Lee-Wen, Shih, Yan-Chung, Tsai, Ping-Hsin, Liu, An-Chi, Hung, Chien-Hui, Liou, Jieh-Yuan, Wang, Shie-Shan
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 10.05.2011
Subjects
Cell Line
Down-Regulation
Gene Expression Regulation, Viral - physiology
Herpesvirus 8, Human - physiology
Human herpesvirus 8
Humans
Immediate-Early Proteins - genetics
Immediate-Early Proteins - metabolism
Infectious Disease
Kaposi's sarcoma-associated herpesvirus
KSHV
Lytic replication
ORF50
ORF50 promoter
Promoter Regions, Genetic
Protein Binding
RNA Interference
Trans-Activators - genetics
Trans-Activators - metabolism
Virus Latency
YY1
YY1 Transcription Factor - genetics
YY1 Transcription Factor - metabolism
YY1
ORF50
Lytic replication
ORF50 promoter
KSHV
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Summary:Abstract Lytic cycle reactivation of Kaposi's sarcoma-associated herpesvirus (KSHV) is initiated by expression of the ORF50 gene. Here we show that YY1 protein specifically binds to the ORF50 promoter (ORF50p) region in vitro and in vivo . After treatment with chemical inducers, including sodium butyrate (SB) and TPA, the levels of YY1 protein are inversely correlated with the lytic induction of KSHV in cells. Overexpression of YY1 completely blocks the ORF50p activation in transient reporter assays, while mutation at the YY1 site in the ORF50p or knockdown of YY1 protein confers an enhancement of the ORF50p activation induced by SB and TPA. YY1 overexpression in a stable cell clone HH-B2(Dox-YY1) also inhibits expression of the ORF50 and its downstream lytic genes. On the other hand, a chimeric YY1 construct that links to its coactivator E1A can disrupt viral latency. These results imply that YY1 is involved in the regulation of KSHV reactivation.
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ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2011.02.013