1995 Fiscal Year Final Research Report Summary
Regulation of differentiation in slime mold cells
Project/Area Number |
06044234
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Research Category |
Grant-in-Aid for international Scientific Research
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Allocation Type | Single-year Grants |
Section | Joint Research |
Research Institution | Okazaki National Research Institutes |
Principal Investigator |
TAKEUCHI Ikuo Okazaki National Research Institutes, 機構長 (90025239)
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Co-Investigator(Kenkyū-buntansha) |
JOHN Bonner プリンストン大学, 名誉教授
RICH Firtel カリフォルニア大学, サンジェゴ校, 教授
VIDYANAND Na インド科学研究所, 教授
MICHEL Veron パスツール研究所, 教授
JEFFERY Will 英国帝国がん研究所, 教授
前田 みね子 大阪大学, 理学部, 助手 (70029700)
OKAMOTO Koji Kyoto University, Faculty of Science, 理学部, 教授 (10029944)
MAEDA Yasuo Tohoku University, Faculty of Science, 理学部, 教授 (50025417)
FIRTEL Richard University of California of SanDiego
BONNER John T. Princeton University
MANJUNDISH Vidyanand Indian Institute of Science
VERON Michel Pasteur Institut
MINEKO Maeda Osaka University, Faculty of Science
WILLIAMS Jeffrey G. Imperial Cancer Research Fund
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Project Period (FY) |
1994 – 1995
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Keywords | cell differentiation / gene expression / cell growth / cell cycle / signal transduction / cellular slime mold |
Research Abstract |
In the development of cellular slime molds, cells aggregate to form a tissue, in which two types of cells (prestalk and prespore) differentiate in the anterior and the posterior parts, respectively.To elucidate regulatory mechanisms of differentiation, we made the following studies. 1.Relation of cell growth and differentiation Whether cells differentiate into either prestalk or prespore cells in the tissue is related to the cell cycle phase at the time of starvation.Putative shift (PS) point from growth to differentiation was determined and genes specifically expressed at the point were examined.Three kinds of genes (Quit 1,2,3) were identified.The Quit gene encodes a cAMP receptor, CAR1 and the Quit2 a new type of calcium-binding protein (CAF-1). 2.Mechanism of stalk cell-inducing factor Cells secrete during development a factor inducing stalk cell differentiation (STIF).The fact that STIF is replaced by 8-bromo-cAMP suggests that STIF acts through protein kinase A (PKA).This possibility was verified, as cells transformed with a dominant negative inhibitor of PKA was incapable of stalk cell formation.STIF activates stalk-specific ecmB gene, but not ecmA gene.The upstream region of ecmB promoter where STTF acts was identified by using cells transformed with various deleted genes. 3.Role of MAP-kinase in signal transduction. Analysis of an aggregateless mutant indicated a MAP-kinase, ERK2 gene has an important role in chemotaxis of cells.ERK2 was activated by extracellular cAMP through membrane receptors, CAR1 and CAR3 and eventually activates adenylate cyclase (AC), without involving heterotrimetric G-proteins.Activation of AC results in an increase in cellular cAMP which in turn inactivates ERK2. Activation of ERK2 is essential for cell growth during the vegetative phase, which is brought about by folic acid and strongly depends on the G proteins.
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