1998 Fiscal Year Final Research Report Summary
Involvement of cell-cell interaction in cell differentiation and morphogenesis
Project/Area Number |
09640772
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
植物生理
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Research Institution | OSAKA UNIVERSITY |
Principal Investigator |
MAEDA Mineko Graduate School of Science Research Associate, 大学院・理学研究科, 助手 (70029700)
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Project Period (FY) |
1997 – 1998
|
Keywords | Dictyostelium / Signal transduction / Cell differentiation / Cyclic AMP / Folic acid / MAP kinase / ERK / G-Protein |
Research Abstract |
Dictyostelium cells chemotax toward folic acid in the vegetative stage and cAMP in the aggregation stage. These chemoattractants have been shown to elicit adenylyl cyclase activation. Recently, it was revealed that MAP-kinase ERK2 is involved in the activation of adenylyl cyclase by extracellular cAMP in Dictyostelium cells (Maeda et al., 1996). We also found that ERK2 is negatively regulated by ras and also regulated by cAMP-dependent protein kinase in a postive feed-back (Aubry et al., 1997). Here, I investigated whether the activation of adenylyl cyclase by folic acid is also mediated by ERK2. In this consequence, I found that ERK2 is transiently activated by folic acid, this activation is mediated through a heterotrimeric G-protein, and the alpha-subunit coupling to this G-protein is G-alpha4 (Maeda& Firtel, 1997). Further, I revealed that monapterin, a derivative of folic acid, also activates ERK2. As monapterin attracts Dictyostelium cells only in the later developmental stages than the aggregation stage, ERK2 activation by monapterin may suggest that cell-cell communication in the late developmental stage is mediated through monapterin-like protein secreted by cells themselves. I also examined the effects of DIE-1 and ammonia, other importants extracellular compounds involved in cell differentiation. Both compounds did not exert any significant effect on ERK2 (unpublished).
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