Effects of deletion of the receptor CrlA on Dictyostelium aggregation and MPBD mediated responses are strain-dependent and not evident in strain Ax2

The polyketide MPBD (4-methyl-5-pentylbenzene-1, 3-diol) is produced by the polyketide synthase SteelyA (StlA) in Dictyostelium discoideum. MPBD is required for appropriate expression of cAMP signalling genes involved in cell aggregation and additionally induces the spore maturation at the fruiting body stage. The MPBD signalling pathway for regulation of cell aggregation is unknown, but MPBD effects on sporulation were reported to be mediated by the G-protein coupled receptor CrlA in D. discoideum KAx3. In this study, we deleted the crlA gene from the same parental strain (Ax2) that was used to generate the MPBD-less mutant. We found that unlike the MPBD-less mutant, Ax2-derived crlA− mutants exhibited normal cell aggregation, indicating that in Ax2 MPBD effects on early development do not require CrlA. We also found that the Ax2/crlA− mutant formed normal spores in fruiting bodies. When transformed with PkaC, both Ax2 and Ax2/crlA− similarly responded to MPBD in vitro with spore encapsulation. Our data make it doubtful that CrlA acts as the receptor for MPBD signalling during the development of D. discoideum Ax2.