Dictyostelium, the RtoA protein links both initial celltypertoA–cells (containing a disruption of the not develop past the mound stage, and have an abnormal ratio of prestalk and prespore cells. RtoA is also involved in fusion of endocytic/exocytic vesicles. Cells lacking RtoA, although having a normal endocytosis rate, have a decreased exocytosis rate and endosomes with abnormally low pHs. RtoA levels vary during the cell cycle, causing a cell-cycle-dependent modulation of parameters such as cytosolic pH (Brazill et al., 2000). To uncover other genes involved in the RtoA-mediated differentiation, we identified genetic suppressors of disrupted two genes, duplication encoding two members of the ATP binding cassette (ABC) transporter superfamily. Disruption of rtoA gene) generally dortoA. One of these suppressorsmdrA1 and mdrA2, a tandem mdrA1/mdrA2 block and suppression of the defect in initial cell type choice caused by loss of the accomplished by re-establishing the link between cell type choice and cell cycle phase. MdrA1 protein is localized to the endosome. disruption of these genes) have an endocytosis rate roughly 70% that of wild-type or mdrA2 that of wild-type. The exocytosis rates of results in release from the developmentalrtoA gene. However, this is notmdrA1–/mdrA2– cells (containing artoA– cells, whereas mdrA1–/–/rtoA– cells have an endocytosis rate roughly 20%mdrA1–/mdrA2–and mdrA1–/mdrA2–/rtoA– are roughly that of wild-type. mdrA1 whereas normal pH. The ability of rescue the cell-type proportion, developmental defects, and endosomal pH defects caused by ability of defects caused by genetic interaction between –/mdrA2– endosomes have an unusually high pH,mdrA1–/mdrA2–/rtoA– endosomes have an almostmdrA1/mdrA2 disruption tortoA disruption, and thertoA disruption to exacerbate the endocytosismdrA1/mdrA2 disruption, suggest artoA, mdrA1 and mdrA2.
In choice and physiological state to cell-cycle phase.