. . . but yeast prion offers clues about evolution

Yeast Prions: Protein Aggregation Is Not Enough

“…In some strains, cells with [PSI + ] prion demonstrated better survival than their non-prion counterparts in the presence of inhibitors of translation or microtubules, heavy metals, low pH, and other deleterious conditions, which of course gives a strong advantage to the [PSI + ] cells. It is likely that some genomic mutations could be suppressed and therefore become silent when termination of translation by Sup35 is partially inactivated in [PSI + ] prion cells (Lindquist 2000; True and Lindquist 2000). [PSI + ] could also reveal previously silent mutations or their combinations.…”

Evolution: The evolvability enigma

“…Indeed, True and Lindquist [2] detected many phenotypic differences between [psi -] strains and isogenic strains that lacked the NM parts of the Sup35 gene, implying that the effects of the NM region cannot arise solely from this regions' capacity to trigger prion formation. Lindquist's view [4] is that the presence of the prion, and its effect of creating novel phenotypes, is of evolutionary importance, even if the creation of evolutionary change has not been causal in the evolution of the prion itself.…”

A Rheostat Model for a Rapid and Reversible Form of Imprinting-Dependent Evolution

“…Lindquist and colleagues have suggested a capacitor model for morphological evolution; in this model, conformational changes in proteins, as influenced by the heat-shock protein Hsp90 (Rutherford and Lindquist 1998), and changes in a yeast prion (Lindquist 2000;True and Lindquist 2000) can provide "an explicit molecular mechanism that assists the process of evolutionary change in response to the environment" (Rutherford and Lindquist 1998, p. 341). Under the capacitor model, altered function of Hsp90 in Drosophila uncovers a multitude of developmental variants that, by selection, can be enriched to become independent of the alteration in Hsp90.…”