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. Author manuscript; available in PMC: 2019 Jul 5.
Published in final edited form as: Mol Cell. 2018 Jul 5;71(1):155–168.e7. doi: 10.1016/j.molcel.2018.06.016

Figure 3: Nucleation barriers govern prion behavior.

Figure 3:

(A) Fits of DAmFRET of known amyloid-forming yeast polypeptides that exhibit bimodal distributions. The inset shows δ ± error. All fits are of [PIN+] cells, except for Rnq1. See also Fig. S3 A, B.

(B)SDD-AGE of Ngr1 PrL and Sla1 PrL in [PIN+] or [pin−] cells. Alternate lanes were intentionally left blank. See also Fig. S3C.

(C) DAmFRET of sesA, showing a bimodal distribution characteristic of prions.

(D) Representative images of ThT-stained cells expressing sesA, positive control Sup35 PrD in [PIN+] and negative control Sup35 PrD in [pin−].

(E) SDD-AGE of sesA in [PIN+] and [pin−] cells. The dashed line indicates the two adjacent lanesshown are spliced from different positions in the gel. See also Fig. S3D.