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. 2018 Mar 6;18(3):foy026. doi: 10.1093/femsyr/foy026

Figure 1.

Figure 1.

Models for the role of [PIN+] in [PSI+] appearance. Two models have been proposed to explain the requirement for [PIN+] in the appearance of [PSI+] in vivo. (A) The most widely accepted model for [PIN+] is that of heterologous nucleus (unfilled pinwheel), stimulating the nucleation of Sup35 (green and blue) by direct interaction. Once nucleated, Sup35 and Rnq1 (the determinant of [PIN+] in laboratory yeast strains) amyloids propagate as separate aggregates. (B) [PIN+] may also promote [PSI+] formation by titrating an inhibitor (green oval) that binds to non-prion state Sup35 and blocks its self-association (step 1). As a variation on the inhibitor model, [PIN+] may titrate the fragmentation machinery (blue hexamer) away from spontaneously forming nascent Sup35 aggregates, allowing them to persist and amplify (step 2). See the text for details on each of the models.