YEAST GCN4 AS A PROBE FOR ONCOGENESIS BY AP-1 TRANSCRIPTION FACTORS - TRANSCRIPTIONAL ACTIVATION THROUGH AP-1 SITES IS NOT SUFFICIENT FOR CELLULAR-TRANSFORMATION

被引:61
作者
OLIVIERO, S
ROBINSON, GS
STRUHL, K
SPIEGELMAN, BM
机构
[1] UNIV PADUA,DIPARTIMENTO BIOL,I-35121 PADUA,ITALY
[2] HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV NAVAL ARCHITECTURE,BOSTON,MA 02115
关键词
YEAST GCN4; JUN; FOS; AP-1 TRANSCRIPTION FACTORS; ONCOGENESIS; CELLULAR TRANSFORMATION;
D O I
10.1101/gad.6.9.1799
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The Jun and Fos oncoproteins belong to the AP-1 family of transcriptional activators and are believed to induce cellular transformation by inappropriately activating genes involved in cell replication. To determine whether transcriptional activation through AP-1 sites is sufficient for transforming activity, we examined the properties of an autonomous and heterologous AP-1 protein, yeast GCN4, in rat embryo fibroblasts. GCN4 induces transcriptional activation through AP-1 sites but, unlike Jun and Fos, fails to induce cellular transformation, in cooperation with Ha-ras. Jun-GCN4 and Fos-GCN4 homodimers independently induce cellular transformation indicating that the amino-terminal regions of Jun and Fos each contain regulatory functions that are required for oncogenesis but are distinct from generic transcriptional activation domains. In addition, these observations have implications for the nature of the oncogenically relevant target genes that respond to Jun and Fos.
引用
收藏
页码:1799 / 1809
页数:11
相关论文
共 65 条
[11]   ACTIVATION OF PROTEIN-KINASE-C DECREASES PHOSPHORYLATION OF C-JUN AT SITES THAT NEGATIVELY REGULATE ITS DNA-BINDING ACTIVITY [J].
BOYLE, WJ ;
SMEAL, T ;
DEFIZE, LHK ;
ANGEL, P ;
WOODGETT, JR ;
KARIN, M ;
HUNTER, T .
CELL, 1991, 64 (03) :573-584
[12]   PROLONGED ACTIVATION OF JUN AND COLLAGENASE GENES BY TUMOR NECROSIS FACTOR-ALPHA [J].
BRENNER, DA ;
OHARA, M ;
ANGEL, P ;
CHOJKIER, M ;
KARIN, M .
NATURE, 1989, 337 (6208) :661-663
[13]   OVEREXPRESSION OF C-JUN, JUNB, OR JUND AFFECTS CELL-GROWTH DIFFERENTLY [J].
CASTELLAZZI, M ;
SPYROU, G ;
LAVISTA, N ;
DANGY, JP ;
PIU, F ;
YANIV, M ;
BRUN, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (20) :8890-8894
[14]   JUN-B DIFFERS IN ITS BIOLOGICAL PROPERTIES FROM, AND IS A NEGATIVE REGULATOR OF, C-JUN [J].
CHIU, R ;
ANGEL, P ;
KARIN, M .
CELL, 1989, 59 (06) :979-986
[15]   FBJ MURINE OSTEO-SARCOMA VIRUS - IDENTIFICATION AND MOLECULAR-CLONING OF BIOLOGICALLY-ACTIVE PROVIRAL DNA [J].
CURRAN, T ;
PETERS, G ;
VANBEVEREN, C ;
TEICH, NM ;
VERMA, IM .
JOURNAL OF VIROLOGY, 1982, 44 (02) :674-682
[16]   FOS AND JUN - THE AP-1 CONNECTION [J].
CURRAN, T ;
FRANZA, BR .
CELL, 1988, 55 (03) :395-397
[17]   TRANSCRIPTION FACTOR INTERACTIONS - SELECTORS OF POSITIVE OR NEGATIVE REGULATION FROM A SINGLE DNA ELEMENT [J].
DIAMOND, MI ;
MINER, JN ;
YOSHINAGA, SK ;
YAMAMOTO, KR .
SCIENCE, 1990, 249 (4974) :1266-1272
[18]   NUCLEOPROTEIN COMPLEXES THAT REGULATE GENE-EXPRESSION IN ADIPOCYTE DIFFERENTIATION - DIRECT PARTICIPATION OF C-FOS [J].
DISTEL, RJ ;
RO, HS ;
ROSEN, BS ;
GROVES, DL ;
SPIEGELMAN, BM .
CELL, 1987, 49 (06) :835-844
[19]   UNREGULATED EXPRESSION OF C-JUN OR C-FOS PROTEINS BUT NOT JUN-D INHIBITS ESTROGEN-RECEPTOR ACTIVITY IN HUMAN BREAST-CANCER DERIVED CELLS [J].
DOUCAS, V ;
SPYROU, G ;
YANIV, M .
EMBO JOURNAL, 1991, 10 (08) :2237-2245
[20]   MOLECULAR CHARACTERIZATION OF THE GCN4-DNA COMPLEX [J].
GARTENBERG, MR ;
AMPE, C ;
STEITZ, TA ;
CROTHERS, DM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (16) :6034-6038