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The cell adhesion glycoproteins, TgrB1 and TgrC1, are essential for  Dictyostelium  development and allorecognition, but it has been impossible to determine whether their pleiotropic roles are due to one common function or to distinct functions in separate pathways. Mutations in the respective genes,  tgrB1  and  tgrC1 , abrogate both development and allorecognition and the defects cannot be suppressed by activation of the cyclic AMP dependent protein kinase PKA, a central regulator of  Dictyostelium  development. Here we report that mutations in genes outside the known PKA pathway partially suppress the  tgrC1 -null developmental defect. We separated the pleiotropic roles of  tgrC1  by testing the effects of a suppression mutation,  stc ins A  under different conditions.  stcA ins   modified only the developmental defect of  tgrC1 –   but not the allorecognition defect, suggesting that the two functions are separable. The suppressor mutant phenotype also revealed that  tgrC1  regulates stalk differentiation in a cell-autonomous manner and spore differentiation in a non-cell-autonomous manner. Moreover,  stcA ins   did not modify the developmental defect of  tgrB1 –  , but the less robust phenotype of  tgrB1 –   obscures the possible role of  stcA  relative to  tgrB1 .

TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition