The inositol cycle in Dictyostelium discoideum was studied both in vitro and in vivo. The results are compared to the inositol cycle as it is known from higher eukaryotes. Although there is a strong resemblance the cycles are different at some essential points. In comparison to higher eukaryotes, in the cycle in D. discoideum the inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] kinase appears to be absent and there are additional phosphatases which hydrolyse Ins(1,4,5)P3 via inositol 4,5-bisphosphate [Ins(4,5)P2] to inositol 4-phosphate (Ins4P). The function of the receptor-stimulated inositol cycle was elucidated using mutants from the fgd A complementation group, which are defective in the G-protein alpha-subunit, responsible for the activation of phosphoinositidase C. These mutants show defects in both chemotaxis and differentiation, suggesting that the stimulation of phosphoinositidase C is the major sensory transduction pathway in D. discoideum.
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