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A novel role of differentiation‐inducing factor‐1 in Dictyostelium development, assessed by the restoration of a developmental defect in a mutant lacking mitogen‐activated protein kinase ERK2
Author(s) -
Kuwayama Hidekazu,
Oyama Masakazu,
Kubohara Yuzuru,
Maeda Mineko
Publication year - 2000
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.2000.00537.x
Subject(s) - adenylyl cyclase , biology , dictyostelium discoideum , dictyostelium , protein kinase a , microbiology and biotechnology , heterotrimeric g protein , mutant , kinase , protein subunit , cyclic adenosine monophosphate , signal transduction , gene , receptor , genetics , g protein
It has been previously reported that the differentiating wild‐type cells of Dictyostelium discoideum secrete a diffusible factor or factors that are able to rescue the developmental defect in the mutant lacking extracellular signal‐regulated kinase 2 (ERK2), encoded by the gene erkB . In the present study, it is demonstrated that differentiation‐inducing factor‐1 (DIF‐1) for stalk cells can mimic the role of the factor(s) and the mechanism of the action of DIF‐1 in the erkB null mutant is also discussed. The mutant usually never forms multicellular aggregates, because of its defect in cyclic adenosine monophosphate (cAMP) signaling. In the presence of 100 n M DIF‐1, however, the mutant cells formed tiny slugs, which eventually developed into small fruiting bodies. In contrast, DIF‐1 never rescued the developmental arrest of other Dictyostelium mutants lacking adenylyl cyclase A (ACA), cAMP receptors cAR1 and cAR3, heterotrimeric G‐protein, the cytosolic regulator of ACA, or the catalytic subunit of cAMP‐dependent protein kinase (PKA‐C). Most importantly, it was found that DIF‐1 did not affect the cellular cAMP level, but rather elevated the transcriptional level of pka during the development of erkB null cells. These results suggest that DIF‐1 may rescue the developmental defect in erkB null cells via the increase in PKA activity, thus giving the first conclusive evidence that DIF‐1 plays a crucial role in the early events of Dictyostelium development as well as in prestalk and stalk cell induction.