Figure 6.

(A) Chemical structures of DIF-1 and DIF-2 and scheme for their actions in inducing stalk cell differentiation and modulating chemotaxis. We assume here that DIF-1 would induce stalk cell differentiation via its receptor DR-1D and subsequent increases in cytoplasmic Ca²⁺ and H⁺ concentrations, at least in part [12,13,14,32], and that DIF-1 would negatively modulate chemotaxis in shallow cAMP gradients via another receptor, DR-1C, whereas DIF-2 would positively modulate chemotaxis in shallow cAMP gradients via its receptor DR-2C. Note that DhkM, another receptor-type Dictyostelium histidine kinase, is involved in DIF-1-induced stalk cell differentiation (autophagic cell death) [36], and DhkM might be DR-1D [37]. (B) Chemical structures of the DIF-1-type molecules, DIF-1(3M) and TM-DIF-1, and scheme for their actions in inducing stalk cell differentiation and inhibiting chemotaxis via the putative DIF receptors. (C) Chemical structures of the DIF-2-type molecules, DIF-1A(+1) and TH-DIF-1, and scheme for their actions in inducing stalk cell differentiation and promoting chemotaxis via the putative DIF receptors. (D) Chemical structures of DIF-2, DIF-1A(+1), and TH-DIF-1, and scheme for their actions in promoting chemotaxis via the DhkC–RdeA–RegA pathway. DhkC might be DR-2C [20].