AI Article Synopsis

  • * The Swi1 protein, which forms the [⁺] prion, is part of a complex that helps regulate yeast genome expression and was studied by comparing strains with and without the prion.
  • * RNA sequencing showed that the presence of the [⁺] prion has a less significant impact on gene expression than deletion of its gene, and while the deletion inhibits translation-related genes, the prion modulates specific metabolic pathways and exhibits both loss-of-function and gain-of-function traits.

Article Abstract

Prions are infectious, self-perpetuating protein conformers. In mammals, pathological aggregation of the prion protein causes incurable neurodegenerative disorders, while in yeast , prion formation may be neutral or even beneficial. According to the prevailing contemporary point of view, prion formation is considered to be a functional inactivation of the corresponding protein whose conformational state shifts from the functional monomeric one to the infectious aggregated one. The Swi1 protein forms the [⁺] prion and belongs to the nucleosome remodeler complex SWI/SNF controlling the expression of a significant part of the yeast genome. In this work, we performed RNA sequencing of isogenic strains grown on the media containing galactose as the sole carbon source. These strains bore the [⁺] prion or had its structural gene deleted. The comparative analysis showed that [⁺] affects genome expression significantly weaker as compared to the deletion. Moreover, in contrast to [⁺], the deletion causes the general inhibition of translation-related genes expression and chromosome I disomy. At the same time, the [⁺] prion exhibits a specific pattern of modulation of the metabolic pathways and some biological processes and functions, as well as the expression of several genes. Thus, the [⁺] prion only partially corresponds to the loss-of-function of and demonstrates several gain-of-function traits.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6471900PMC
http://dx.doi.org/10.3390/genes10030212DOI Listing

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