The role of histone modifications in Fusarium oxysporum pathogenicity

寄主特有形式的尖孢镰刀菌（formae speciales, f.sp）在广泛的农艺相关作物上引起血管性枯萎病。单个菌株的宿主范围很窄，感染依赖于一组特定的小分泌蛋白，即效应物。番茄病原菌F. oxysporum F. sp. lycopersici （Fol）的基因组测序显示了11条保守的核心染色体和4条谱系特异性的辅助染色体。谱系特异性的14号染色体携带所有6个（木质部分泌的）致病性所需的效应基因。未发表的实验表明，foll谱系特异性区域构成兼性异染色质。这些区域在镰刀菌种之间或镰刀菌的f. sp.之间尤其多样，并且在转录上一般是沉默的。在藤黑镰刀菌中，兼性异染色质的特征是组蛋白(H)赖氨酸(K)修饰H3K36me3和H3K27me3。我已经证明，ffash1介导的H3K36me3的缺失导致抑制性H3K27me3的积累，并导致相应区域（亚端粒，副染色体）的频繁丢失。这些机制将在Fol中进一步研究，特别是关于谱系特异性区域的稳定性，以及对植物致病性和效应基因表达的影响。此外，转录因子Sge1 （SIX基因表达1）是大多数效应基因表达所必需的，因此对Fol致病性至关重要。通过检测FoSge1突变体的H3甲基化和乙酰化标记，评估FoSge1在6个基因染色质水平调控中的作用。

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Unpublished experiments have indicated that Fol lineage-specific regions constitute facultative heterochromatin.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.