A network model governing spore formation, dormancy, and germination in Dictyostelium discoideum

The regulation of terminal differentiation of Dictyostelium discoideum has previously been poorly understood. It is a complex mixture of signaling components, cytoskeletal effectors, and metabolic changes. In developing a network model of spore formation, dormancy, and germination, a schematic framework has been developed that incorporates all of the components into one coherent model. At the center of that model, Protein kinase A (Pka) acts as the master regulator. Stimulating Pka activity using cAMP analogues or overexpression of the catalytic subunit suppress the loss of the dual specificity MAP kinase SpIA. Furthermore, increased levels of Pka also restore viability to spIA− null spores. In previous studies, Actin tyrosine phosphorylation has been shown to be a central marker for spore formation. The control of this process is unknown. Compound such as discadenine, the autoinhibitor may control some aspects of this process. During germination, the actin cytoskeleton is rapidly mobilized from its dormant state. Actin and the actin binding protein participate in both the maintenance of dormancy as well as the activation of the cytoskeleton during germination. During germination, massive trehalase stores are rapidly mobilized to provide the necessary energy. Trehalase, the enzyme responsible for this process has been purified from Dictyostelium. A putative gene encoding this protein has also been cloned. Together, the results presented here help establish a model of signaling networks that govern spore dynamics.