The role of histone modifications in Fusarium oxysporum pathogenicity

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Host-specific forms (formae speciales, f. sp.) of Fusarium oxysporum cause vascular wilt disease on a broad range of agronomically relevant crops. Individual strains have a narrow host range, and infection relies on a specific set of small secreted proteins, i.e. effectors. Genome sequencing of the tomato pathogen F. oxysporum f. sp. lycopersici (Fol) revealed eleven conserved core chromosomes and four lineage-specific, accessory chromosomes. Lineage-specific chromosome 14 harbors all SIX (secreted in xylem) effector genes required for pathogenicity.Unpublished experiments have indicated that Fol lineage-specific regions constitute facultative heterochromatin. Such regions are especially diverse among Fusarium species or among f. sp. of F. oxysporum, and transcriptionally silent in general. In Fusarium fujikuroi, facultative heterochromatin is characterized by the histone (H) lysine (K) modifications H3K36me3 and H3K27me3. I have shown that depletion of FfAsh1-mediated H3K36me3 resulted in an accumulation of repressive H3K27me3, and in frequent loss of the respective regions (subtelomeres, accessory chromosome). These mechanisms will be further studied in Fol, especially concerning the stability of lineage-specific regions, and the influence on pathogenicity and effector gene expression in planta.Furthermore, the transcription factor Sge1 (SIX gene expression 1) is required for expression of most effector genes, and is therefore essential for Fol pathogenicity. The role of FoSge1 in the chromatin-level regulation of SIX genes will be assessed, by testing H3 methylation and acetylation marks in FoSGE1 mutants.