Masison D C, Wickner R B
Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD 20892-0830, USA.
Science. 1995 Oct 6;270(5233):93-5. doi: 10.1126/science.270.5233.93.
The genetic properties of the [URE3] non-Mendelian element of Saccharomyces cerevisiae suggest that it is a prion (infectious protein) form of Ure2p, a regulator of nitrogen catabolism. In extracts from [URE3] strains, Ure2p was partially resistant to proteinase K compared with Ure2p from wild-type extracts. Overexpression of Ure2p in wild-type strains induced a 20- to 200-fold increase in the frequency with which [URE3] arose. Overexpression of just the amino-terminal 65 residues of Ure2p increased the frequency of [URE3] induction 6000-fold. Without this "prion-inducing domain" the carboxyl-terminal domain performed the nitrogen regulation function of Ure2p, but could not be changed to the [URE3] prion state. Thus, this domain induced the prion state in trans, whereas in cis it conferred susceptibility of the adjoining nitrogen regulatory domain to prion infections.
酿酒酵母中[URE3]非孟德尔遗传元件的遗传特性表明，它是氮代谢调节因子Ure2p的一种朊病毒（传染性蛋白质）形式。与野生型提取物中的Ure2p相比，[URE3]菌株提取物中的Ure2p对蛋白酶K具有部分抗性。在野生型菌株中过表达Ure2p会使[URE3]出现的频率增加20至200倍。仅过表达Ure2p的氨基末端65个残基会使[URE3]诱导频率增加6000倍。没有这个“朊病毒诱导结构域”，羧基末端结构域执行Ure2p的氮调节功能，但不能转变为[URE3]朊病毒状态。因此，该结构域在反式中诱导朊病毒状态，而在顺式中它使相邻的氮调节结构域易受朊病毒感染。
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