Nucleic Acids Research, 1990, Vol. 18, No. 10 2929-2938
© 1990
MOLECULAR BIOLOGY |
The embryonal carcinoma stem cell Ela-like activity involves a differentiation-regulated transcription factor
Laboratory of Eukaryotic Molecular Genetics, National Institute for Medical Research The Ridgeway, Mill Hill, London NW7 1AA 1Department of Microbiology and Immunology, Northwestern University Medical School 303 East Chicago Avenue, Chicago, IL 60611, USA
Received January 9, 1990. Accepted April 19, 1990.
Murine F9 embryonal carcinoma (EC) stem cells have an Ela-like transcription activity that is undetectable in F9 cells differentiated to parietal endoderm-like cells (F9-PE). The Ela-inducible adenovlrus E2A promoter has been used to further define this activity and we show that in vitro the transcription of this promoter in F9 EC and F9-PE cell extracts reflects the regulation in vivo. In EC cell extracts several trans-acting protein factors bind to E2A promoter sequences. A distal domain containing a CRE binds proteins present in F9 EC, F9-PE and Hela cell extracts. Sequences between 71 and 50 define a multiplicity of binding activities, termed DRTF1, all of which are down regulated as EC stem cells differentiate. DRTF2, a low abundance, regulated binding activity requires DNA sequences that overlap those required by DRTF1. The CRE and the DRTF1 binding site compete for transcription in vitro, indicating that In EC cell extracts the respective proteins function as positively acting, binding site dependent transcription factors. Comparison of DRTF1 with the previously defined HeLa cell factor E2F, induced during adenovirus infection, indicates that although both factors recognise the same region of the promoter there are clear differences between them. These data indicate that multiple factors are necessary for efficient transcription of the E2A promoter in F9 EC cell extracts and suggest that DRTF1 is responsible, at least in part, for the developmental regulation of the cellular Ela-like activity.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
C. H. Choi, Z. Rapti, V. Gelev, M. R. Hacker, B. Alexandrov, E. J. Park, J. S. Park, N. Horikoshi, A. Smerzi, K. O. Rasmussen, et al. Profiling the Thermodynamic Softness of Adenoviral Promoters Biophys. J., July 15, 2008; 95(2): 597 - 608. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Vara, K. A. Bicknell, C. H. Coxon, and G. Brooks Inhibition of E2F Abrogates the Development of Cardiac Myocyte Hypertrophy J. Biol. Chem., June 6, 2003; 278(24): 21388 - 21394. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Wasylyk and B. Wasylyk Defect in the p53-Mdm2 Autoregulatory Loop Resulting from Inactivation of TAFII250 in Cell Cycle Mutant tsBN462 Cells Mol. Cell. Biol., August 1, 2000; 20(15): 5554 - 5570. [Abstract] [Full Text] |
||||
![]() |
R. M. Gill and P. A. Hamel Subcellular Compartmentalization of E2F Family Members Is Required for Maintenance of the Postmitotic State in Terminally Differentiated Muscle J. Cell Biol., March 20, 2000; 148(6): 1187 - 1202. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Takeda, H. Kurachi, T. Yamamoto, H. Homma, K. Adachi, K. Morishige, A. Miyake, and Y. Murata Alternative Signaling Mechanism of Leukemia Inhibitory Factor Responsiveness in a Differentiating Embryonal Carcinoma Cell Endocrinology, July 1, 1997; 138(7): 2689 - 2696. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. Hao, L Alphey, L. Bandara, E. Lam, D Glover, and N. La Thangue Functional conservation of the cell cycle-regulating transcription factor DRTF1/E2F and its pathway of control in Drosophila melanogaster J. Cell Sci., January 9, 1995; 108(9): 2945 - 2954. [Abstract] [PDF] |
||||
![]() |
M. Rosner, M. Vigano, P. Rigby, H Arnheiter, and L. Staudt Oct-3 and the beginning of mammalian development Science, July 12, 1991; 253(5016): 144 - 145. [PDF] |
||||






