pdsA, a gene involved in the production of active phosphodiesterase during starvation of Dictyostelium discoideum amoebae

Summary

Upon starvation, amoebae of the mutant strain HPX235 are unable to aggregate. Previous work has shown that this aggregateless character was associated with a nearly complete block in the production of the phosphodiesterase by these cells. Aggregation of the HPX235 amoebae can be induced with exogenous phosphodiesterase. In the present work, we show that both the aggregateless character and the block in phosphodiesterase production appear to result from the same recessive mutation, allocated to I.g.IV. Two other mutant strains displaying a comparable phenotype (HPX262 and HP594) were shown by complementation to belong to the same locus pdsA. Unlike wild type cells, the mutants of the locus pdsA cannot be induced to produce phosphodiesterase following treatment of the cells with exogenous cAMP, whether exogenous phosphodiesterase is present or not in the starvation buffer. It is concluded that pdsA is either the structural gene for the phosphodiesterase or a controlling element whose integrity is required for phosphodiesterase production. Mutations in pdsA share secondary effects among which the abnormally low production of the phosphodiesterase inhibitor. However, this effect can be overcome upon addition of exogenous phosphodiesterase, and most likely results from the lack of cAMP hydrolysis.

The late development is also affected in pdsA mutants. Aggregates formed in the presence of exogenous phosphodiesterase cannot culminate normally. This suggests that the level of cAMP hydrolysis also plays a role during the late stages of development of Dictyostelium discoideum.