The prestalk-prespore pattern in cellular slime molds.

In cellular slime molds the slugs become divided into two regions with different properties, and anterior prestalk-zone and a posterior prespore zone. Although the cells in these zones are normally destined to form the stalk cells and spores of the fruiting body, respectively, they are not irreversibly committed to one sort of differentiation or the other during the slug stage. The volume ratio of the two zones remains almost constant over a wide range of slug sizes. If the prestalk-prespore pattern is distrubed by removing tissue from the slug, conversion of tissue from prestalk to prespore or vice versa occurs as necessary to restore a normal pattern with normal proportions. Conversions also occur in both directions during normal development. The initial formation of the prestalk-prespore pattern may well involve sorting-out, but other mechanisms must be invoked to account for regulation. We describe three different models of the generation of the prestalk-prespore pattern, the'cell-contact model' of McMahon, in which pattern is created by interactions of cells with their immediate neighbors, the 'positional-information model' of various authors, in which pattern formation involves an overall gradient and a gradient-reading mechanism, and the 'activator-inhibitor model' of Gierer and Meinhardt, in which the prestalk-prespore pattern is formed by a system of diffusible substances that affect one another's production. The activator-inhibitor model is the most successful of the models at describing the known features of the prestalk-prespore pattern. The various models lead to a number of distinctive predictions. According to the cell-contact model, small transplants may cause gross changes in the prestalk-prespore pattern, and mutants may exist which severely disrupt pattern formation even if diluted with a large excess of wild-type cells. Positional-information models predict the existence of 'gradient-reading mutants'; slugs that are a mixture of such mutants and wild-type cells would show two prestalk-prespore boundaries, one at the mutant and one at the normal position. Both the activator-inhibitor model and some versions of the positional-information model predict that small transplants will sometimes induce accessory prestalk or prespore zones; the quantitative characteristics of these effects may allow one to make a case in favor of one or other of the two models. Finally, the activator-inhibitor model leads one to expect that mutants may be isolated which normally show accessory prestalk or prespore zones. A search for these phenomena may help determine whether the activator-inhibitor model will continue to enjoy its present preeminent position.