[No authors listed]
Currently, several protein-based genetic determinants, or prions, are described in yeast, and several hundred prion candidates have been predicted. Importantly, many known and potential prion proteins regulate transcription; therefore, prion induction should affect gene expression. While it is generally believed that the prion phenotype should mimic the deletion phenotype, this rule has exceptions. Formed by the transcription factor Sfp1p, [ISP(+) ] is one such exception as the [ISP(+) ] and sfp1Î strains differ in many phenotypic traits. These data suggest that effects of prion formation by a transcription factor and its absence may affect gene expression in a different way. However, studies addressing this issue are practically absent. Here, we explore how [ISP(+) ] affects gene expression and how these changes correspond to the effect of SFP1 deletion. Our data indicate that the [ISP(+) ]-related expression changes cannot be explained by the inactivation of Sfp1p. Remarkably, most Sfp1p targets are not affected in the [ISP(+) ] strain; instead, the genes upregulated in the [ISP(+) ] strain are enriched in Gcn4p and Aft1p targets. We propose that Sfp1p serves as a part of a regulatory complex, and the activity of this complex may be modulated differently by the absence or prionization of Sfp1p.
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