The CCAAT-binding transcription factor (CTF)/nuclear factor I (NF-I) group of cellular DNA-binding proteins recognizes the sequence GCCAAT and is implicated in eukaryotic transcription, as well as DNA replication. Molecular analysis of human CTF/NF-I cDNA clones revealed multiple mRNA species that contain alternative coding regions, apparently as a result of differential splicing. Expression and functional analysis established that individual gene products can bind to GCCAAT recognition sites and serve as both promoter-selective transcriptional activators and initiation factors for DNA replication. The interaction between CTF2 and p53/p73 was shown to modulate their ability to regulate transcription of their respective target genes. In the present paper, we report that p53 down-regulates the activity of the high mobility group 1 (HMG1) gene promoter, whereas p73α up-regulates the activity of this promoter. Furthermore, CTF2 transactivates p53-induced p21 promoter activity, but inhibits p73α-induced p21 promoter activity. Using deletion mutants, we found that the DNA-binding domains of both p53 and p73α are required for physical interaction with CTF2 via the regions between amino acid residues 161 and 223, and 228 and 312 respectively. CTF2 enhances the DNA-binding activity of p53 and inhibits the DNA-binding activity of p73α. These results provide novel information on the functional interplay between CTF2 and p53/p73 as important determinants of their function in cell proliferation, apoptosis, DNA repair and cisplatin resistance.
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April 2003
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Research Article|
April 15 2003
Physical interaction of tumour suppressor p53/p73 with CCAAT-binding transcription factor 2 (CTF2) and differential regulation of human high-mobility group 1 (HMG1) gene expression
Hidetaka URAMOTO;
Hidetaka URAMOTO
∗Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Hiroto IZUMI;
Hiroto IZUMI
∗Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Gunji NAGATANI;
Gunji NAGATANI
∗Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Haruki OHMORI;
Haruki OHMORI
†Second Department of Surgery, Shimane Medical University, Izumo, Shimane 693-8501
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Naofumi NAGASUE;
Naofumi NAGASUE
†Second Department of Surgery, Shimane Medical University, Izumo, Shimane 693-8501
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Tomoko ISE;
Tomoko ISE
∗Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Takeshi YOSHIDA;
Takeshi YOSHIDA
∗Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Kosei YASUMOTO;
Kosei YASUMOTO
‡Second Department of Surgery, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Kimitoshi KOHNO
Kimitoshi KOHNO
1
∗Department of Molecular Biology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
1To whom correspondence should be addressed (e-mail k-kohno@med.uoeh-u.ac.jp).
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Publisher: Portland Press Ltd
Received:
October 22 2002
Revision Received:
January 14 2003
Accepted:
January 20 2003
Accepted Manuscript online:
January 20 2003
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London ©2003
2003
Biochem J (2003) 371 (2): 301–310.
Article history
Received:
October 22 2002
Revision Received:
January 14 2003
Accepted:
January 20 2003
Accepted Manuscript online:
January 20 2003
Citation
Hidetaka URAMOTO, Hiroto IZUMI, Gunji NAGATANI, Haruki OHMORI, Naofumi NAGASUE, Tomoko ISE, Takeshi YOSHIDA, Kosei YASUMOTO, Kimitoshi KOHNO; Physical interaction of tumour suppressor p53/p73 with CCAAT-binding transcription factor 2 (CTF2) and differential regulation of human high-mobility group 1 (HMG1) gene expression. Biochem J 15 April 2003; 371 (2): 301–310. doi: https://doi.org/10.1042/bj20021646
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