Deep Field / case
Prion
PrP^Sc in neural tissue templates its misfolded conformation onto native PrP^C through direct protein–protein contact, achieving massive redundant inscription across independent molecular substrates—Witness-function without the regulatory Canon that stabilises genetically encoded folding. Chaperones, quality-control degradation, and feedback canalisation are absent; templating is spontaneous in the relevant conformational landscape, bearing zero regulatory investment unlike Photosystem II's thirty-minute repair cycle. What propagates is conformational pattern, not a viable phenotype compressed by selective governance. The pattern floods tissue: replication without canalisation. Strain incoherence, conformational drift under temperature and pH shifts genetic canalisation would absorb, and spongiform degeneration follow. Cease substrate supply and propagation stalls; remove Canon coupling and pathology is the diagnostic signature—fluent replication whose characteristic failure is ungoverned flood rather than channelled persistence.
spontaneous conformational templating without regulatory investment
Replication without canalisation; conformational drift and pathology
Local graph
Typed relations
Source anchors
- Ch06 - The Stabilisation Engine