Regulatory gene interactions controlling discoidin lectin expression in Dictyostelium discoideum

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Abstract
Genetic studies have revealed a network of three unlinked regulatory genes that control the developmental expression of the family of endogenous lectins in Dictyostelium discoideum. Mutations in the disA and disB loci have a null phenotype and do not express the discoidin I or II lectins. The third mutation, drsA, is a second‐site suppressor of the disB mutation, which restores expression of all lectin species. Cells carrying this mutation express the discoidin lectins during growth, which is in contrast to wild‐type cells in which lectin synthesis is developmentally regulated. In addition to this basic level of genetic control, the conditions of growth dramatically influence the patterns of discoidin expression. Growth‐phase wild‐type cells do not express lectin if the cells are grown on plates in association with bacteria. However, wild‐type cells growing in bacterial suspensions express high levels of lectin during growth. Synthesis of the discoidin lectins in growing cells is sensitive to the levels of extracellular cyclic adenosine monophosphate (cAMP) and folic acid. These results suggest that the drsA mutation renders cells insensitive to cAMP and/or folate and thus allows expression of lectin during growth.