Dictyostelium cells can move rapidly towards a source of cyclic-AMP (cAMP),
This chemoattractant is detected by G-protein-linked receptors, which trig
ger a signalling cascade including a rapid influx of Ca2+. We have disrupte
d an inositol 1,4,5-trisphosphate (InsP(3)) receptor-like gene, iplA, to pr
oduce null cells in which Ca2+ entry in response to chemoattractants is abo
lished, as is the normal increase in free cytosolic Ca2+ ([Ca2+](c)) that f
ollows chemotactic stimulation. However, the resting [Ca2+](c) is similar t
o wild type. This mutant provides a test for the role of Ca2+ influx in bot
h chemotaxis and the signalling cascade that controls it. The production of
cyclic-GMP and cAMP, and the activation of the MAP kinase, DdERK2, trigger
ed from the cAMP receptor, are little perturbed in the mutant; mobilization
of actin into the cytoskeleton also follows similar kinetics to wild type,
Mutant cells chemotax efficiently towards cAMP or folic acid and their sen
sitivity to cAMP is similar to wild type, Finally, they move at similar spe
eds to wild-type cells, with or without chemoattractant, We conclude that C
a2+ signalling is not necessary for chemotaxis to cAMP.