Mutations in the Cc.rmt1 gene encoding a putative protein arginine methyltransferase alter developmental programs in the basidiomycete Coprinopsis cinerea.

We characterized two developmental mutants of Coprinopsis cinerea, Apa56 and Sac29, newly isolated from a homokaryotic fruiting strain, 326 (Amut Bmut pab1-1), after restriction enzyme-mediated integration (REMI) mutagenesis. Both Apa56 and Sac29 exhibited slower mycelial growth than the parental wild-type strain and failed to initiate fruiting when grown on standard malt extract-yeast extract-glucose medium under 12 h light/12 h dark cycle. Both mutants exhibited unusual differentiation in aerial hyphae: differentiated hyphae lacked clamp connections and exhibited irregular shapes. The differentiated hyphae were similar to the component cells of hyphal knots, but did not form hyphal knots: they spread as dense mycelial mats. When the carbon source (glucose) in the medium was substituted with sucrose or galactose, both strains formed as many hyphal knots as the parental wild type. The hyphal knots formed, however, did not develop into fruiting-body initials, but developed into sclerotia. Molecular genetic analysis revealed that the gene, designated Cc.rmt1, is disrupted by REMI mutagenesis and is responsible for the phenotypes in both mutants. Cc.rmt1 is predicted to encode a putative protein arginine methyltransferase, some homologs of which have been shown to be involved in the regulation of gene expression in eukaryotes.