Supplemental Material for Edskes et al., 2018

Supplemental Methods_figures_tables.pdf - Provides a detailed description of the culture conditions, induction of <i>Hermes</i> transposition, selection of colonies carrying a transposition, extraction of cellular DNA, PCR amplification and isolation of the junction points between transposon and chromosomal insertion site, next-generation sequencing of these sites, and analysis of the data by visual display and by counting insertions per open reading frame. <br><br> Exon Intron Counts.xlsx - Gives the insertions in every yeast open reading frame, distinguishing exons from introns where appropriate.<br><br>Sorted Hits.xlsx - Gives prominent hits sorted by functional group, “TY gag-pol Counts.xlsx comparing insertions in the Ty retrotransposons at different locations in the genome. <br><br>Count Insertions in ORFs and Introns.txt - The Python program used for counting insertions. <br><br>LUGsIGV-InsertDistributions.pptx - Is a slide show of insert distributions in each of 500 genes for which insertions were recovered more frequently in [ure-o] than in [URE3] cultures

Protein conformation templating mechanism.

<p>The in-register parallel amyloid architecture naturally suggests a mechanism for transfer of conformation information from molecules in the filament to those joining the filament. H-bonding or hydrophobic favorable interactions among identical side chains require in-register alignment for the interactions. This directs the monomer joining the end of the filament to have its folds/turns at the same residues as previous molecules in the filament. Different prion variants have folds/turns at different locations, but each is faithfully propagated by this mechanism. Modified from [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004584#ppat.1004584.ref006" target="_blank">6</a>].</p

Btn2p sequesters prion amyloid filaments, curing the prion.

<p>Btn2p gathers filaments of Ure2p amyloid (the [URE3] prion) to a single site in the cell, possibly the endosome. If the prion has a low seed number then even the normal levels of Btn2p are sufficient to sequester nearly all of the seeds, so that daughter cells without seeds, and therefore cured of the prion, are often produced.</p