Table 1.
Variant-Defining Condition/Trait | Prions Affected | Mechanism | Relation to Strong/Weak? | Refs. |
---|---|---|---|---|
Strength of phenotype (strong/weak) | [PSI+], [URE3] | high filament number adsorb more prion protein | [10,28,29] | |
Prion stability | [PSI+], [URE3] | high filament number insures both daughters infected | Strong often stable, weak often unstable; exceptions | [10,28,29] |
prion toxicity (all variants detrimental but the degree varies) | [PSI+], [URE3] | [PSI+]: depletion of Sup35p (essential) [URE3]: toxic effect of amyloid form |
unknown | [33] |
interspecies or intraspecies barriers | [PSI+], [URE3] | inefficient binding to amyloid of different protein sequence | [34,35,36] | |
lethality or prion loss in Sis1p partial deletions | [PSI+] | unknown | strong variant lethal; weak variant lost | [37,38] |
Sse1p required for propagation or generation | [PSI+] | strong variant weakened, weak variant lost | [39,40] | |
curing by normal levels of Hsp104 | [PSI+] | some of both are cured; no relation to seed # | [41] | |
curing by normal levels of Btn2p | [URE3] | filaments sequestered by Btn1p, Hsp42p | All cured variants are weak, but some weak variants not cured | [42] |
curing by normal levels of Cur1p | [URE3] | unknown | All cured variants are weak, but some weak variants not cured | [42] |
curing by normal levels of Upf1,2,3 | [PSI+] | complex formation with Sup35p | no relation to strong/weak | [43] |
curing by normal levels of Siw14p | [PSI+] | limits 5PP-IP5 levels | unknown | [44] |