Fruiting body development in fungi is a complex cellular differentiation process that is controlled by more than 100 developmental genes. Mutants of the filamentous fungus Sordaria macrospora showing defects in fruiting body formation are pertinent sources for the identification of components of this multicellular differentiation process. Here we show that the sterile mutant pro11 carries a defect in the pro11 gene encoding a multimodular WD40 repeat protein. Complementation analysis indicates that the wild-type gene or Cterminally truncated versions of the wild-type protein are able to restore the fertile phenotype in mutant pro11. PRO11 shows significant homology to several vertebrate WD40 proteins, such as striatin and zinedin, which seem to be involved in Ca 2 -dependent signaling in cells of the central nervous system and are supposed to function as scaffolding proteins linking signaling and eukaryotic endocytosis. Cloning of a mouse cDNA encoding striatin allowed functional substitution of the wild-type protein with restoration of fertility in mutant pro11. Our data strongly suggest that an evolutionarily conserved cellular process controlling eukaryotic cell differentiation may regulate fruiting body formation. Fruiting bodies are highly complex multicellular structures that are generated during the sexual life cycle of filamentous fungi. In ascomycetous fungi, such as Neurospora crassa, Sordaria macrospora, and Aspergillus nidulans, fruiting bodies are termed ascomata and enclose sexual meiosporangia (asci) and meiospores (ascospores). While ascospores arise from hyphae during the meiotic cycle, all tissues forming the fruiting body arise from haploid, nondikaryotic hyphae. This feature distinguishes fruiting body formation in ascomycetes clearly from that in basidiomycetous fungi, in which dikaryotic hyphae are involved in both, the meiotic cycle and fruiting body formation (for a review, see reference 26). The sexual life cycle of ascomycetes can be either heteroth
