Regulation of host‐infection ability in the grass‐symbiotic fungus Epichloë festucae by histone H3K9 and H3K36 methyltransferases

Abstract

Summary Recent studies have identified key genes that control the symbiotic interaction between Epichloë festucae and Lolium perenne . Here we report on the identification of specific E. festucae genes that control host infection. Deletion of setB , which encodes a homologue of the H3K36 histone methyltransferase Set2/KMT3, reduced histone H3K36 trimethylation and led to severe defects in colony growth and hyphal development. The E. festucae Δ clrD mutant, which lacks the gene encoding the homologue of the H3K9 methyltransferase KMT1, displays similar developmental defects. Both mutants are completely defective in their ability to infect L. perenne . Alleles that complement the culture and plant phenotypes of both mutants also complement the histone methylation defects. Co‐inoculation of either Δ setB or Δ clrD with the wild‐type strain enables these mutants to colonize the host. However, successful colonization by the mutants resulted in death or stunting of the host plant. Transcriptome analysis at the early infection stage identified four fungal candidate genes, three of which encode small‐secreted proteins, that are differentially regulated in these mutants compared to wild type. Deletion of crbA , which encodes a putative carbohydrate binding protein, resulted in significantly reduced host infection rates by E. festucae .

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