Fig. 7. A two-component model for the survival mechanism of Cin cells. The model presented comprises two key elements: (1) a suppressor gene for calnexin/Cnx1p essentiality (scx1⁺, for suppressor of cnx1⁺); and (2) a regulator of scx1 activity that is designated Cif1p, for calnexin-independence factor). In the calnexin-dependent state, the protein encoded by cif1 is present in the cell in its native conformer Cif1p, negatively regulating scx1 activity on cnx1⁺ essential function on its putative target (symbolised as `?'). However, under particular conditions, such as the presence of hcd_Cnx1p, the Cif1p protein could convert into an alternative conformer [cif] unable to inhibit scx1 activity. Under these latter conditions, scx1 could complement the essential function of calnexin/Cnx1p on its target `?'. This would allow the loss of episomal cnx1⁺ in a cnx1 + pcnx1⁺ strain when grown under non-selective conditions since cnx1⁺ activity on target `?' would be no longer vital, and thereby giving rise to calnexin-independent cells (Cin). The [cif] conformer would provoke further conversion of Cif1p molecules into the [cif] form by an `autocatalytic' process, such as structural replication, which can be inherited during mitosis and meiosis, and that can be transmitted by transformation. These features of [cif] would constitute the basis for the dominance and the inheritance of the Cin state. Details of this model are given in the Discussion section.