1989 Fiscal Year Final Research Report Summary
Function of regulatory factors of transcription and DNA replication in relation to the F9 cell differentiation.
| Project/Area Number |
63440027
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ITO Yoshiaki Kyoto Univ., Inst. Virus Res., Professor, ウイルス研究所, 教授 (80004612)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Yota Kyoto Univ., Inst., Virus Res., Postdoc. Fellow, ウイルス研究所, 日本学術振興会特別研
SATAKE Masanobu Kyoto Univ., Inst. Virus Res., Assoc. Prof., ウイルス研究所, 助教授 (50178688)
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| Project Period (FY) |
1988 – 1989
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| Keywords | F9 cell / cell differentiation / polyomavirus / enhancer / transcriptional regulator / replicational regulator / AP1 / c-Ha-ras oncogene |
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| Research Abstract |
F9 cells can be induced to differentiate into endoderm-like cells by retinoic acid treatment. We analyzed the function of several regulatory factors of transcription and DNA replication in relation to the F9 cell differentiation.
1. The enhancer of a mutant of polyomavirus, F9-5000, had a 24bp deletion and could function in F9 cells as well as in those induced to differentiate by retinoic acid. The DELTAF9-5000 element corresponds to the deleted region of the enhancer. This element functioned to suppress gene expression in F9 cells and bound a factor, PEBP4, which was thought to be responsible for the repression. In differentiated cells, however, the same element enhanced gene expression and bound transcriptional activator, PEBP2, as well as PEBP4. The recognition sequence of PEBP2 partly overlapped with that of PEBP4. PEBP3 (dephosphorylated form of PEBP2) and PFBP4 were actually shown to compete for the site for binding. Interplay of a ubiquitous negative factor and differentiation-induced positive factor may represent one aspect of the gene regulation during embryonic development.
2. A transcriptional activator, AP1, is a heterodimer of the products of nuclear proto-oncogenes, c-jun and c-fos and is undetectable in F9 cells. The activated c-Ha-ras oncogene was found to induce the AP1 activity in F9 cells. This induction appeared to be due to the induction of c-jun gene transcription. Both the activated c-Ha-ras and c-jun genes induced the differentiation of F9 cells to endoderm-like cells.AP1 appeared to play a key role at the initial stage of the Fg cell differentiation.
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