YY1 represses human papillomavirus type 16 transcription by quenching AP-1 activity

被引:101
作者
OConnor, MJ [1 ]
Tan, SH [1 ]
Tan, CH [1 ]
Bernard, HU [1 ]
机构
[1] NATL UNIV SINGAPORE, INST MOL & CELL BIOL, LAB PAPILLOMAVIRUS BIOL, SINGAPORE 117548, SINGAPORE
关键词
D O I
10.1128/JVI.70.10.6529-6539.1996
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
YY1 is a multifunctional transcription factor that has been shown to regulate the expression of a number of cellular and viral genes, including the human papillomavirus (HPV) oncogenes E6 and E7. In this study, we have analyzed the YY1-mediated repression of the HPV type 16 (HPV-16) E6-E7 promoter. A systematic analysis to identify YY1 sites present in the HPV-16 long control region showed that of 30 potential YY1 binding motifs, 24 bound purified recombinant YY1 protein, but only 10 of these were able to bind YY1 when nuclear extracts of HeLa cells were used. Of these, only a cluster of five sites, located in the vicinity of an AP-1 motif, were found to be responsible for repressing the HPV-16 P97 promoter. All five sites were required for repression, the mutation of any one site giving rise to a four- to sixfold increase in transcriptional activity. The target for YY1-mediated repression was identified as being a highly conserved AP-1 site, and we propose that AP-1 may represent a common target for YY1 repression. We also provide data demonstrating that YY1 can bind the transcriptional coactivator CREB-binding protein and propose a potentially novel mechanism by which YY1 represses AP-1 activity as a result of this YY1-CREB-binding protein interaction.
引用
收藏
页码:6529 / 6539
页数:11
相关论文
共 80 条
[1]   CLONING AND FUNCTIONAL-ANALYSIS OF SPLICED ISOFORMS OF HUMAN NUCLEAR FACTOR I-X - INTERFERENCE WITH TRANSCRIPTIONAL ACTIVATION BY NFI CTF IN A CELL-TYPE-SPECIFIC MANNER [J].
APT, D ;
LIU, YC ;
BERNARD, HU .
NUCLEIC ACIDS RESEARCH, 1994, 22 (19) :3825-3833
[2]   NUCLEAR FACTOR-I AND EPITHELIAL CELL-SPECIFIC TRANSCRIPTION OF HUMAN PAPILLOMAVIRUS TYPE-16 [J].
APT, D ;
CHONG, T ;
LIU, YC ;
BERNARD, HU .
JOURNAL OF VIROLOGY, 1993, 67 (08) :4455-4463
[3]   E1A-ASSOCIATED P300 AND CREB-ASSOCIATED CBP BELONG TO A CONSERVED FAMILY OF COACTIVATORS [J].
ARANY, Z ;
SELLERS, WR ;
LIVINGSTON, DM ;
ECKNER, R .
CELL, 1994, 77 (06) :799-800
[4]   CBP-INDUCED STIMULATION OF C-FOS ACTIVITY IS ABROGATED BY E1A [J].
BANNISTER, AJ ;
KOUZARIDES, T .
EMBO JOURNAL, 1995, 14 (19) :4758-4762
[5]  
Bannister AJ, 1995, ONCOGENE, V11, P2509
[6]   IDENTIFICATION OF A NEGATIVE REGULATORY DOMAIN IN THE HUMAN PAPILLOMAVIRUS TYPE-18 PROMOTER - INTERACTION WITH THE TRANSCRIPTIONAL REPRESSOR-YY1 [J].
BAUKNECHT, T ;
ANGEL, P ;
ROYER, HD ;
HAUSEN, HZ .
EMBO JOURNAL, 1992, 11 (12) :4607-4617
[7]  
BAUKNECHT T, 1995, J VIROL, V69, P1
[8]   TRANSCRIPTIONAL CONTROL AND CELL-TYPE SPECIFICITY OF HPV GENE-EXPRESSION [J].
BERNARD, HU ;
APT, D .
ARCHIVES OF DERMATOLOGY, 1994, 130 (02) :210-215
[9]   THE PREDOMINANT MESSENGER-RNA CLASS IN HPV16-INFECTED GENITAL NEOPLASIAS DOES NOT ENCODE THE E6 OR THE E7 PROTEIN [J].
BOHM, S ;
WILCZYNSKI, SP ;
PFISTER, H ;
IFTNER, T .
INTERNATIONAL JOURNAL OF CANCER, 1993, 55 (05) :791-798
[10]   TRANSCRIPTION OF THE TRANSFORMING GENES OF THE ONCOGENIC HUMAN PAPILLOMAVIRUS-16 IS STIMULATED BY TUMOR PROMOTORS THROUGH AP1 BINDING-SITES [J].
CHAN, WK ;
CHONG, T ;
BERNARD, HU ;
KLOCK, G .
NUCLEIC ACIDS RESEARCH, 1990, 18 (04) :763-769