科研之友
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摘要
The budding yeast, Saccharomyces cerevisiae, harbors several prions that are transmitted as altered, heritable protein conformations. [SWI+] is one such prion whose determinant is Swi1, a subunit of the evolutionarily conserved chromatin-remodeling complex SWI/SNF. Despite the importance of Swi1, the molecular events that lead to [SWI+] prionogenesis remain poorly understood. In this study, we have constructed floccullin-promoter-based URA3 reporters for [SWI+] identification. Using these reporters, we show that the spontaneous formation frequency of [SWI+] is significantly higher than that of [PSI+] ( prion form of Sup35). We also show that preexisting [PSI+] or [PIN+] ( prion form of Rnq1), or overproduction of Swi1 prion-domain (PrD) can considerably promote Swi1 prionogenesis. Moreover, our data suggest a strain-specific effect of overproduction of Sse1 - a nucleotide exchange factor of the molecular chaperone Hsp70, and its interaction with another molecular chaperone Hsp104 on [SWI+] maintenance. Additionally, we show that Swi1 aggregates are initially ring/ribbon-like then become dot-like in mature [SWI+] cells. In the presence of [PSI+] or [PIN+], Swi1 ring/ribbon-like aggregates predominantly colocalize with the Sup35 or Rnq1 aggregates; without a preexisting prion, however, such colocalizations are rarely seen during Swi1-PrD overproduction-promoted Swi1 prionogenesis. We have thus demonstrated a complex interacting mechanism of yeast prionogenesis.
- 出版日期2017-4
- 单位西北大学
