Abstract
Although transcription factors are prevalent among yeast prion proteins, the role of prion-mediated transcriptional regulation remains elusive. Here, we show that the yeast prion [SWI+] abolishes flocculin (FLO) gene expression and results in a complete loss of multicellularity. Further investigation demonstrates that besides Swi1, multiple other proteins essential for FLO expression, including Mss11, Sap30, and Msn1 also undergo conformational changes and become inactivated in [SWI+] cells. Moreover, the asparagine-rich region of Mss11 can exist as prion-like aggregates specifically in [SWI+] cells, which are SDS resistant, heritable, and curable, but become metastable after separation from [SWI+]. Our findings thus reveal a prion-mediated mechanism through which multiple regulators in a biological pathway can be inactivated. In combination with the partial loss-of-function phenotypes of [SWI+] cells on non-glucose sugar utilization, our data therefore demonstrate that a prion can influence distinct traits differently through multi-level regulations, providing insights into the biological roles of prions.
Original language | English (US) |
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Pages (from-to) | 2865-2878 |
Number of pages | 14 |
Journal | Cell reports |
Volume | 13 |
Issue number | 12 |
DOIs | |
State | Published - Dec 29 2015 |
Keywords
- SWI/SNF
- Saccharomyces cerevisiae
- Swi1
- amyloids
- filamentous growth
- flocculin
- multicellularity
- prion
- protein conformation change
- protein-aggregation
- yeast
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)