Hsp104-Dependent Remodeling of Prion Complexes Mediates Protein-Only Inheritance (original) (raw)
Figure 5
Loss of Sup35-GFP[_PSI+_] Fluorescence in Wild-Type Cells Corresponds to Redistribution of Existing Fusion Protein to New Prion Complexes
(A) The metabolic stability of Sup35-GFP was analyzed in [_PSI+_] (SY81) or [_psi−_] (SY87) yeast lysates upon inhibition of new protein synthesis with cycloheximide. An anti-Sup35 immunoblot is shown along with an anti-Pgk1 immunoblot of the same membrane as a control for loading.
(B) Shown are representative images (n = 7) of a wild-type zygote (SY360 × SY581) constitutively expressing untagged SUP35 from its endogenous locus (left image) and of the same zygote following the formation of a second daughter and first granddaughter (right image). The Sup35-GFP in these cells is that existing at the time of mating as described in Figure 2A.
(C) FRAP recovery curves for a wild-type zygote (SY360 × SY581; black circles) and its daughter (white circles), as described in (B), are shown. The respective recovery times are 0.92 s (R2 = 0.85) and 0.95 s (R2 = 0.84).