Wickner R B, Masison D C, Edskes H K
Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, MD 20892-0830, USA.
Yeast. 1995 Dec;11(16):1671-85. doi: 10.1002/yea.320111609.
[URE3] is a non-Mendelian genetic element that mimics recessive mutations in the chromosomal URE2 gene making cells derepressed for nitrogen catabolic enzymes. [PSI] is a non-Mendelian enhancer of readthrough of translational termination similar in its effects to some mutations in the chromosomal SUP35 gene. Three lines of evidence led to the proposal that both [URE3] and [PSI] are prions, infectious proteins analogous to the scrapie agent mediating transmissible spongiform encephalopathies of mammals. 1) Both [PSI] and [URE3] are reversibly curable. 2) [PSI] propagation requires SUP35 and [URE3] propagation requires URE2 with recessive chromosomal mutants having the same phenotypes as the presence of the respective dominant non-Mendelian element. 3) Overproduction of Sup35p and Ure2p increases the frequency of cells acquiring [PSI] or [URE3], respectively.
[URE3]是一种非孟德尔遗传元件，它模拟染色体上URE2基因中的隐性突变，使细胞中氮分解代谢酶的表达去阻遏。[PSI]是翻译终止通读的非孟德尔增强子，其作用类似于染色体上SUP35基因中的某些突变。三条证据线索促使人们提出[URE3]和[PSI]都是朊病毒，即类似于介导哺乳动物传染性海绵状脑病的瘙痒病病原体的传染性蛋白质。1）[PSI]和[URE3]都可被可逆治愈。2）[PSI]的传播需要SUP35，[URE3]的传播需要URE2，隐性染色体突变体具有与相应显性非孟德尔元件存在时相同的表型。3）Sup35p和Ure2p的过量表达分别增加了细胞获得[PSI]或[URE3]的频率。
