Fig. 7.

Model for the regulation of filamentation by Sch9. (A) Wild-type cells grown under hypoxia at high CO₂ levels. Under hypoxia, Efg1 acts as a repressor of filamentous growth (14, 33, 34), but Czf1 limits its repressor activity (4, 14). Under high CO₂ levels, the PKA isoforms Tpk1 and Tpk2 are activated, presumably by bicarbonate-mediated activation of adenylate cyclase (20). It is proposed that PKA is downregulated in certain environments (surface growth, temperatures of <37°C) by the Tor1-Sch9 pathway to prevent hypha formation. It is yet unclear if Sch9 increases Efg1 repressor activity by inactivation of Czf1, as shown, or by another mechansm, e.g., by blocking PKA activity. Ace2 is required for hypoxic filamentation (24) by a yet-unknown mechanism. (B) Lack of Sch9 or Tor1 activity during hypoxic growth under high CO₂ fails to repress the CO₂-triggered increase in PKA activity, leading to hyperfilamentation. (C) A moderate level of Efg1 repressor activity under hypoxic growth and low CO₂ levels suffices to block hypha formation at low PKA activity.