Article ID Journal Published Year Pages File Type
2180829 Fungal Genetics and Biology 2013 8 Pages PDF
Abstract

We characterized a Coprinopsis cinerea mutant strain, Spe20, defective in fruiting initiation, which was isolated after restriction enzyme-mediated integration (REMI) mutagenesis of a homokaryotic fruiting strain, 326. A plasmid rescue followed by complementation experiments, RACE, and cDNA analyses revealed that the gene, a mutation of which is responsible for the phenotype, is predicted to encode a protein that exhibits a high similarity to yeast Snf5p, a key component of the chromatin remodeling complex SWI/SNF, and named Cc.snf5. Cc.Snf5 is, however, different from Snf5p in that the former has, in addition to an Snf5 domain comprising N-terminal repeat1 (rp1) and C-terminal repeat2 (rp2) subdomains in a middle region, a GATA Zn-finger domain in a C-terminal region. In strain Spe20, plasmid pPHT1 used for REMI is inserted in the ORF encoding rp2. This raised the possibility that in strain Spe20, the disrupted Cc.Snf5 is functionally active albeit incompletely because it retains rp1. Thus, we disrupted the whole SNF5 domain and its downstream peptide and found that the disruption results in inhibition of not only fruiting initiation but also dikaryon development, a prerequisite for fruiting. We also found that specific disruption of the Zn-finger domain results in inhibition of fruiting initiation. These results indicate that Cc.Snf5 plays an essential role in sexual development of C. cinerea.

► We identified a Coprinopsis cinerea mutant defective in fruiting. ► The gene responsible for the mutation encodes a Snf5 protein named Cc.Snf5. ► Cc.Snf5 contains a GATA Zn-finger domain. ► Cc.Snf5 is a component of the SWI/SNF chromatin remodeling complex. ► Different targeted disruptions of Cc.Snf5 affect sexual development differently.

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