Transcriptional regulation of the c-jun gene by retinoic acid and E1A during differentiation of F9 cells.

Abstract

Differentiation of mouse F9 embryonal carcinoma (EC) cells can be induced by exposure to retinoic acid (RA) or by expression of adenovirus E1A. The transcription of the c‐jun gene is stimulated by either RA or E1A. We report here that both RA and E1A strongly induce the expression of chloramphenicol acetyltransferase (CAT) from c‐jun promoter/CAT reporter construct (c‐jun/CAT), which is stably integrated into F9 cells, in a manner that is independent of both copy number and integration locus. The induction of c‐jun/CAT expression is observed in undifferentiated F9 cells, but not in differentiated F9 cells, adenovirus‐infected F9 cells or HeLa cells. Deletion analysis of the promoter region of the c‐jun gene indicates that the sequence elements required for the RA‐ and E1A‐mediated induction are identical and they have been defined as a region of 145 bp between −190 and −46 of the 5′ flanking region of c‐jun. This RA and E1A response element (RERE) contains five variants of the motif CGCGGTGACGNT. The upstream two motifs are adjacent and extend in opposite directions, creating an imperfect palindrome. The downstream four motifs are located at 35 or 36 bp intervals in the same orientation. Substitution and insertion analysis indicates that these motifs and their regular intervals are important for the activity of the RERE.

Rapid Effects of Retinoic Acid on CREB and ERK Phosphorylation in Neuronal Cells

“…Induction of c-Jun by RA is not restricted to A126-1B2 cells. Thus, activation of c-jun transcription is observed during RA-induced differentiation of embryonic carcinoma cells (Yang-Yen et al, 1990;Kitabayashi et al, 1992). Also in this case RA appears to induce transcription by a RARE-independent mechanism through complexes that include ATF-2 and the coactivator CBP/p300 (Kawasaki et al, 1998).…”

MAZ, a Myc-associated zinc finger protein, is essential for the ME1a1-mediated expression of the c-myc gene during neuroectodermal differentiation of P19 cells

“…Retinoic acid (Sigma Chemical Co.) for induction of di erentiation was added to cultured cells in monolayers at 1610 76 M. For induction of neural di erentiation of P19 cells, cells were cultured in bacteriological-grade dishes (Becton Dickinson, Franklin Lakes, NJ, USA) in the presence of RA at 1610 76 M for 2 days, transferred to tissue culture-grade dishes (Corning, Corning, NY, USA), and cultured in the absence of RA for another 2 days as described elsewhere McBurney et al, 1982;Edward et al, 1983). Transient and stable transfections and assays of chloramphenicol acetyltransferase (CAT) activity were performed as described elsewhere (Kitabayashi et al, 1992). The extent of conversion of chloramphenicol to its acetylated form was determined with a Bio-Imaging analyzer (model BAS 2000; Fuji, Tokyo, Japan).…”

“…The extent of conversion of chloramphenicol to its acetylated form was determined with a Bio-Imaging analyzer (model BAS 2000; Fuji, Tokyo, Japan). b-Galactosidase activity was assayed as described by Kitabayashi et al (1992). The ratio of CAT activity to the activity of b-galactosidase was used for normalization of results.…”

Suppression of serum-induced c-jun expression by activated Ki-ras in human colon cancer cells

“…The proto-oncogene c-jun shows numerous cellular phenotypes such as oncogenic transformation, differentiation, and the response to toxic agents Kitabayashi et al, 1991;Verheij et al, 1996). The diversity of functions by c-Jun will be due to its combinatorial association with other members of transcriptional factors that exhibited distinct DNA binding specificity (Nakabeppu et al, 1988;Hai and Curren, 1991).…”

“…These results raised the possibility that activated Ki-ras will be involved in the deregulation of other immediate early genes, such as c-jun, which is involved in growth, differentiation, and apoptosis (Kitabayashi et al, 1991;Verheij et aL, 1996). c-Jun belongs to AP-1 family, whose expression is rapidly stimulated by serum, forming homodimers and/or heterodimers with other AP-1 families .…”