Abstract
Because of mechanistic similarities between prion propagation in mammals and fungi, Tuite and Serio recently proposed (The prion hypothesis: from biological anomaly to basic regulatory mechanism. Nature Rev. Mol. Cell Biol. 11, 823–833 (2010))1 that similarly to fungal prions, which are thought to act as phenotype regulators, prions in mammals should be considered as a basic regulatory mechanism instead of a biological anomaly. However, by considering the behaviour of prions, we argue that the fact that mammalian and fungal prions use a similar mechanism of conformational conversion is not enough to suggest that they are not just infectious agents.
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