Derkatch I L, Bradley M E, Zhou P, Liebman S W
Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, 900 S. Ashland Avenue, Chicago, IL 60304, USA.
Curr Genet. 1999 Mar;35(2):59-67. doi: 10.1007/s002940050433.
We have previously described different variants of the yeast prion [PSI+] that can be obtained and maintained in the same genetic background. These [PSI+] variants, which differ in the efficiency of nonsense suppression, mitotic stability and the efficiency of curing by GuHCl, may correspond to different [PSI+] prion conformations of Sup35p or to different types of prion aggregates. Here we investigate the effects of overexpressing a mutant allele of SUP35 and find different effects on weak and strong [PSI+] variants: the suppressor phenotype of weak [PSI+] factors is increased, whereas the suppressor effect of strong [PSI+] factors is reduced. The SUP35 mutation used was originally described as a "Psi no more" mutation (PNM2) because it caused loss of [PSI+]. However, none of the [PSI+] variants in the strains used in our study were cured by PNM2. Indeed, when overexpressed, PNM2 induced the de novo appearance of both weak and strong [PSI+] variants with approximately the same efficiency as the overexpressed wild-type SUP35 allele. Our data suggest that the change in the region of oligopeptide repeats in the Sup35p N-terminus due to the PNM2 mutation modifies, but does not impair, the function of the prion domain of Sup35p.
我们之前描述过酵母朊病毒[PSI+]的不同变体，它们可以在相同的遗传背景中获得并维持。这些[PSI+]变体在无义抑制效率、有丝分裂稳定性和GuHCl治愈效率方面存在差异，可能对应于Sup35p的不同[PSI+]朊病毒构象或不同类型的朊病毒聚集体。在这里，我们研究了过表达SUP35突变等位基因的影响，发现对弱[PSI+]和强[PSI+]变体有不同的影响：弱[PSI+]因子的抑制表型增加，而强[PSI+]因子的抑制作用降低。所使用的SUP35突变最初被描述为“不再有Psi”突变（PNM2），因为它导致了[PSI+]的丧失。然而，我们研究中使用的菌株中的任何[PSI+]变体都没有被PNM2治愈。实际上，当PNM2过表达时，它诱导了弱[PSI+]和强[PSI+]变体的从头出现，其效率与过表达的野生型SUP35等位基因大致相同。我们的数据表明，由于PNM2突变导致的Sup35p N端寡肽重复区域的变化改变了但并未损害Sup35p朊病毒结构域的功能。
