TRANSCRIPTION OF DJUN FROM DROSOPHILA-MELANOGASTER IS POSITIVELY REGULATED BY DTF-1, AP-1, AND CREB BINDING-SITES

Citation
Gl. Wang et Es. Goldstein, TRANSCRIPTION OF DJUN FROM DROSOPHILA-MELANOGASTER IS POSITIVELY REGULATED BY DTF-1, AP-1, AND CREB BINDING-SITES, Experimental cell research, 214(1), 1994, pp. 389-399
Citations number
68
Categorie Soggetti
Oncology,"Cytology & Histology
Journal title
ISSN journal
00144827
Volume
214
Issue
1
Year of publication
1994
Pages
389 - 399
Database
ISI
SICI code
0014-4827(1994)214:1<389:TODFDI>2.0.ZU;2-R
Abstract
Djun is the homolog of the mammalian proto-oncogene jun in D. melanoga ster, where it encodes a component of an AP-1-like nuclear DNA binding protein, or transcription factor. Djun, unlike its vertebrate counter parts, contains an intron in its 5' noncoding region. The expression o f Djun in cultured Schneider line 2 cells is controlled by multiple ci s-acting elements in its promoter region and the 5' noncoding region o f the transcription unit. A 43-bp 5' upstream promoter region is neces sary for the transcription activity of Djun. Deletion of this fragment decreased transcriptional activity by 67-fold. This region includes a TATA box and a sequence similar to the Drosophila transcription facto r 1 (DTF-1) consensus sequence (GCAACAT/cG/c). A large DNase I footpri nt covering both the DTF-1 binding site and the TATA box was detected in this region when incubated with nuclear extract from Drosophila emb ryos, suggesting interactions with related transcription factors. This 43-bp sequence alone, containing the DTF-1 binding site and TATA box, however, is not sufficient for transcription activity. An 80-bp seque nce including the start of transcription has considerable basal activi ty. An intragenic region containing an AP-1 site and a CRE site modula tes or fine tunes activity of the promoter. Its activity as an enhance r is reduced when moved upstream in either orientation. An extragenic region containing two AP-1 sites similarly affects promoter activity. (C) 1994 Academic Press, inc.