Figure 8
Model for O 2 regulation of development and dependence on the Skp1 modification pathway. Cells form loose aggregates that condense into tight aggregates by a Skp1 associated, O2 dependent mechanism based on submerged development studies (Figures 4D, 7A-2). At a conventional air-water interface (upper track, depicted by dashed line), the exposed apical surface supports maximal O2 transport which is proposed to induce tip formation whose smaller radius of curvature encourages even more O2 transport, stabilizing the tip as an organizer and the zone where cells differentiate as prestalk cells. The Skp1 modification pathway, under regulation of O2 and other factors, regulates culmination and sporulation at the air-water interface. Under submerged conditions (lower track), metabolism consumes O2, which becomes depleted owing to slow diffusion in the unstirred cultures. In this isotropic and hypoxic environment, all (not just apical) surface cells become prestalk cells and, in the absence of a polarizing O2 gradient, cells differentiate in situ and those that sense the lowest O2 level (which occurs in the center) become spores. O2 action may be complementary to NH3, a volatile inhibitor that is generated during development and is preferentially lost from the same surfaces by diffusion (see Discussion).