Mammalian amyloidogenic proteins PrP and Aβ(1–42) do not induce formation of the Sup35 prion in trans. Overexpression of PrP(90–230) or Aβ(1–42) (A) or of their respective fusions to GFP (B) from the copper-inducible promoter, PCUP1, induces [PSI+] formation in the [psi−
pin−] strain neither on its own nor in the presence of excess Sup35N (produced under the control of the galactose inducible promoter, PGAL). The QN-rich prion-inducing protein Lsb2 fused to GFP (B) is shown as a positive control. Cultures were pre-incubated on the medium containing additional CuSO4 at a concentration of 0, 50, and 150 μm from left to right. The protein levels for PrP(90–230), PrP(90–231)-GFP, and Aβ(1–42)-GFP are shown in Fig. S1A; the formation of detergent-resistant aggregates by PrP(90–231)-GFP and Aβ(1–42)-GFP and shown in Fig. S1B.