title: As a toxin dies a prion comes to life: A tentative natural history of the [Het-s] prion.
abstract: A variety of signaling pathways, in particular with roles in cell fate and host defense, operate by a prion-like mechanism consisting in the formation of open-ended oligomeric signaling complexes termed signalosomes. This mechanism emerges as a novel paradigm in signal transduction. Among the proteins forming such signaling complexes are the Nod-like receptors (NLR), involved in innate immunity. It now appears that the [Het-s] fungal prion derives from such a cell-fate defining signaling system controlled by a fungal NLR. What was once considered as an isolated oddity turns out to be related to a conserved and widespread signaling mechanism. Herein, we recall the relation of the [Het-s] prion to the signal transduction pathway controlled by the NWD2 Nod-like receptor, leading to activation of the HET-S pore-forming cell death execution protein. We explicit an evolutionary scenario in which formation of the [Het-s] prion is the result of an exaptation process or how a loss-of-function mutation in a pore-forming cell death execution protein (HET-S) has given birth to a functional prion ([Het-s]).
authors.affiliation: a Non-self recognition in Fungi; Institut de Biochimie et de Génétique Cellulaire; UMR 5095; CNRS - Université de Bordeaux ; Bordeaux cedex , France.
authors.forename: Asen
authors.initials: A
authors.lastname: Daskalov
authors.forename: Sven J
authors.initials: SJ
authors.lastname: Saupe
mesh_terms: D020816:Amino Acid Motifs; D019143:Evolution, Molecular; D011328:Prions / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000737:chemistry / Q000378:metabolism; D015398:Signal Transduction; D014118:Toxins, Biological / Q000378:metabolism*
chemical_list: D011328:Prions; D011956:Receptors, Cell Surface; D014118:Toxins, Biological
keywords: [Het-s]; amyloid; cell death; exaptation; incompatibility; nod-like receptors