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Significance The [URE3] prion (infectious protein) is an amyloid (filamentous polymer) of Ure2p. Overproduction of Btn2p or Cur1p cure this prion, and Btn2p colocalizes with Ure2p aggregates in the curing process. We show that most [URE3] variants arising in the absence of Btn2p and Cur1p are cured by restoring the normal levels of these two proteins. The variants cured by normal levels of Btn2p and Cur1p are those with low seed number, a low number of heritable particles, consistent with seed aggregation, and sequestration as the curing mechanism. These Btn2p and Cur1p antiprion proteins are members of the Hook protein family, metazoan members of which have roles in microtubule-dependent movement of organelles and aggregates in the cell.

Normal levels of the antiprion proteins Btn2 and Cur1 cure most newly formed [URE3] prion variants