Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0830, USA.
Proc Natl Acad Sci U S A. 2011 Mar 29;108(13):5337-41. doi: 10.1073/pnas.1102762108. Epub 2011 Mar 14.
[PSI(+)] is a prion of the essential translation termination factor Sup35p. Although mammalian prion infections are uniformly fatal, commonly studied [PSI(+)] variants do not impair growth, leading to suggestions that [PSI(+)] may protect against stress conditions. We report here that over half of [PSI(+)] variants are sick or lethal. These "killer [PSI(+)]s" are compatible with cell growth only when also expressing minimal Sup35C, lacking the N-terminal prion domain. The severe detriment of killer [PSI(+)] results in rapid selection of nonkiller [PSI(+)] variants or loss of the prion. We also report variants of [URE3], a prion of the nitrogen regulation protein Ure2p, that grow much slower than ure2Δ cells. Our findings give a more realistic picture of the impact of the prion change than does focus on "mild" prion variants.
[PSI(+)]是必需翻译终止因子 Sup35p 的朊病毒。尽管哺乳动物朊病毒感染是一致致命的，但通常研究的 [PSI(+)]变体不会损害生长，这导致了 [PSI(+)]可能对应激条件具有保护作用的建议。我们在这里报告说，超过一半的 [PSI(+)]变体是病态或致命的。这些“杀手 [PSI(+)]”只有在表达最小的 Sup35C 时才与细胞生长兼容，而 Sup35C 缺乏 N 端朊病毒结构域。杀手 [PSI(+)]的严重损害导致快速选择非杀手 [PSI(+)]变体或丧失朊病毒。我们还报告了氮调节蛋白 Ure2p 的朊病毒 [URE3]的变体，其生长速度比 ure2Δ 细胞慢得多。我们的发现比关注“温和”朊病毒变体更真实地描绘了朊病毒变化的影响。
