The role of histone modifications in Fusarium oxysporum pathogenicity

特定于宿主的形式(Formae Speciales，f.sp.)尖孢镰刀菌在广泛的农艺作物上引起维管萎缩病。个别菌株的宿主范围很窄，感染依赖于一组特定的小分泌蛋白，即效应器。番茄枯萎病菌基因组序列测定。番茄属植物有11条保守的核心染色体和4条谱系特有的副染色体。谱系特异的14号染色体包含致病所需的所有六个效应基因(分泌在木质部中)。未发表的实验表明，Fol谱系特异性区域构成兼性异染色质。这样的区域在不同的镰刀菌种或不同的赤霉菌中尤其不同。尖孢镰刀菌属，一般转录沉默。在Fujikuroi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，并导致各自区域(端粒下、辅助染色体)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区的稳定性，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(六个基因表达1)是大多数效应基因表达所必需的，因此在Fol致病中是必不可少的。通过测试FoSGE1突变体中的H3甲基化和乙酰化标记，将评估FoSge1在六个基因染色质水平调节中的作用。

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Unpublished experiments have indicated that Fol lineage-specific regions constitute facultative heterochromatin.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