Abstract
A human cDNA clone for ERM, a member of the ets gene family, has been obtained by polymerase chain reaction with degenerate primers corresponding to highly conserved regions within an Ets DNA binding domain. ERM mRNA is expressed ubiquitously. The gene was mapped to chromosome 3q27. In in vivo transient-expression assays, ERM induced transcription more efficiently from a synthetic element containing both an ets-binding site (EBS) and a cyclic AMP response element (CRE) than from one containing an EBS alone. The activation of a synthetic EBS-CRE site by ERM was likely to involve a leucine zipper protein capable of dimerizing with CRE-BP1 leucine zipper. Indeed, ERM and c-Jun synergistically activated the EBS-CRE without making an apparent ternary complex. The synergy between c-Jun and ERM may be attributed to the enhancing effect of c-Jun on the transcription activity of ERM, because c-Jun increased ERM transcription activity by more than 20-fold in an assay system using a variety of fusion proteins between a Gal4 DNA-binding domain and a portion of ERM. This enhancing effect of c-Jun required the amino-terminal portion of ERM.
Highlights
The ets oncogene family members are involved in gene activation through interactions with other gene products [1,2,3,4]
Putative ets-binding sites (EBS)1 have been identified in a variety of promoters or enhancers, including the ets-1 promoter [21], interleukin-2 gene enhancer (NFAT-1) [18], polyomavirus enhancer (PEA3) [22], moloney sarcoma virus long terminal repeat [23], SV40 enhancer [15], human T-cell leukemia virus type I long terminal repeat [24], human immunodeficiency virus type 2 long terminal repeat [25], human herpes simplex virus ICP4 enhancer [16, 26], stromelysin promoter [27], T-cell receptor ␣ and  enhancers (28 –30), c-fos promoter [2, 10, 31], immunoglobulin 3Ј enhancer [32], immunoglobulin heavy chain intron enhancer [33], and granulocyte macrophage colony-stimulating factor promoter [34]
Direct interaction between the Ets family members and other transcription factors has been demonstrated in many cases, including Ets-1/Sp1 on the EBSs of human T-cell leukemia virus type I long terminal repeat [36], GABP␣/GABP on the herpes simplex virus ICP4 enhancer [16, 26], PU.1/NF-EM5 on the immunoglobulin 3Ј enhancer [32], p62 ternary complex factor (p62TCF)/serum response factor on the c-fos serum response element (SRE) [2, 10, 31], and Ets-1/CBF on the T-cell receptor  chain E2 and E3 enhancers [29]
Summary
The ets oncogene family members are involved in gene activation through interactions with other gene products [1,2,3,4]. The members of the Ets family often show functional synergism with other transcription factors to achieve efficient activation of such target genes through an EBS and adjacent DNA sequences [10, 22, 35]. A factor(s) binding to the PEA3 site of polyoma virus enhancer and collagenase promoter acts synergistically with AP1 to express maximal transcription activity [22]. During the effort to clone a constitutive JEBS-binding protein, we recloned a member of the ets gene family, ERM [39], belonging to the PEA3 subfamily. We show that ERM and c-Jun synergistically activate transcription from a synthetic element containing an EBS and a CRE without apparent cooperative binding to the corresponding site. ERM is the first ets gene family member that acts synergistically with c-Jun and whose transcriptional activity is enhanced by c-Jun
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