Non-mendelian inheritance of the HET-s prion or HET-s prion domains determines the het- S spore killing system in Podospora anserina

Abstract

Two alleles of the het-s/ S locus occur naturally in the filamentous fungus Podospora anserina, het- s and het- S. The het- s encoded protein can form a prion that propagates a self-perpetuating amyloid aggregate, resulting in two phenotypes for the het- s strains. The prion-infected [Het-s] shows an antagonistic interaction to het- S whereas the prion-free [Het-s*] is neutral in interaction to het- S. The antagonism between [Het-s] and het- S is seen as heterokaryon incompatibility at the somatic level and as het- S spore killing in the sexual cycle. Two different domains of the HET-s and HET-S proteins have been identified, and a structure–function relationship has been established for interactions at the somatic level. In this study, we correlate accumulation of the HET-s and HET-S proteins (visualized using GFP) during the sexual cycle with timing of het- S spore abortion. Also, we present the structure–function relationship of the HET-s domains for interactions in the sexual cycle. We show that the constructs that ensure het- s incompatibility function in somatic mycelium are also active in het- S spore killing in the sexual cycle. In addition, paternal prion transmission and het- S spore killing has been found with the HET-s(157–289) truncated protein. The consequences of the unique transition from a coenocytic to a cellular state in the sexual phase and the timing, and localization of paternal and maternal HET-s and HET-S expression that are pertinent to prion transmission, and het-S spore killing are elaborated. These data further support our previously proposed model for het- S spore killing.