Neurospora crassa has been a model for studying DNA methylation and other epigenetic factors such as histone modifications in filamentous fungi. The first plenary speaker, Eric Selker (University of Oregon, USA) has made major contributions to understanding fungal DNA methylation and histone methylation associated with DNA methylation (H3K9me3, a heterochromatic mark). Selker first described how he identified and characterized genes encoding proteins that directly or indirectly influence DNA methylation in N. crassa by combining genetic and biochemical approaches in his earlier studies . He then summarized his recent works showing that distinct DNA methylation and histone deacetylation complexes are required for heterochromatin formation and gene silencing . He also discussed the presence and the role of H3K27me3 in N. crassa. Considering that H3K27me3 is absent in the chromatin of Saccharomyces cerevisiae and many filamentous fungi, its evolution and function in fungal species will be of great interest.
Zachary Lewis (University of Gerogia, USA) gave a concurrent session talk about γH2A and heterochromatin in N. crassa. γH2A is a phosphorylated form of H2A and recruits chromatin-binding proteins that stabilize stalled replication forks or promote DNA repair . Through a ChIP-seq experiment, he showed that γH2A is enriched in heterochromatin domains in a DIM-5 (a histone methyltransferase for H3K9me3) dependent manner (unpublished). However, γH2A is required neither for H3K9 methylation nor DNA methylation. Given that γH2A is a biomarker for double strand break induced by DNA damage, his data suggest that proper heterochromatin formation is important for DNA repair and replication.
In fungi, it was known that secondary metabolite (SM) gene cluster are silenced by the formation of facultative heterochromatin. In another concurrent session, Joseph Strauss (BOKU University, Austria) reported a genetic and biochemical investigation of two histone demethylases that are involved in the regulation of SM clusters in Aspergillus nidulans: KdmA and KdmB (unpublished). KdmA acts as a repressor of SM clusters by binding to H3K9me3 and demethylating H3K36me3, whereas KdmB acts as an activator by binding to H3K4me3 and demethylating H3K9me3. Deletion of the genes followed by transcriptome and ChIP analysis showed that the enzymes really regulate transcription of genes at the tested SM clusters.