Abstract
Dimorphism or morphogenic conversion is exploited by several pathogenic fungi and is required for tissue invasion and/or survival in the host. We have identified a homolog of a master regulator of this morphological switch in the plant pathogenic fungus Fusarium oxysporum f. sp. lycopersici. This non-dimorphic fungus causes vascular wilt disease in tomato by penetrating the plant roots and colonizing the vascular tissue. Gene knock-out and complementation studies established that the gene for this putative regulator, SGE1 (SIX Gene Expression 1), is essential for pathogenicity. In addition, microscopic analysis using fluorescent proteins revealed that Sge1 is localized in the nucleus, is not required for root colonization and penetration, but is required for parasitic growth. Furthermore, Sge1 is required for expression of genes encoding effectors that are secreted during infection. We propose that Sge1 is required in F. oxysporum and other non-dimorphic (plant) pathogenic fungi for parasitic growth.
Highlights
The fungus Fusarium oxysporum is found in both agricultural and non-cultivated soils throughout the world
Isolation and characterization of SGE1 and FoPAC2 In an insertional mutagenesis screen aimed at identifying genes involved in pathogenicity a non-pathogenic mutant (5G2) and one severely reduced in pathogenicity (101E1) were identified that both carried a single T-DNA insertion into the ORF of FOXG_10510 [9], hereafter called SGE1 (SIX Gene Expression 1)
Many genes have been identified that play a role during pathogenesis, many of which are linked to general strain fitness
Summary
The fungus Fusarium oxysporum is found in both agricultural and non-cultivated soils throughout the world. The pathogenic isolates, grouped into formae specialis depending on their host range [1,2], cause wilt or rot disease in important agricultural and ornamental plant species, such as tomato, banana, cotton and tulip bulbs, thereby causing serious problems in commercial crop production [3,4]. In the absence of plant roots F. oxysporum survives in the soil either as dormant propagules (chlamydospores) or by growing saprophytically on organic matter [1,8]. When growing on roots of a suitable host F. oxysporum appears to switch from a saprophyte into a pathogen. F. oxysporum likely undergoes reprogramming of gene expression. Examples are SIX1, encoding a small secreted protein, and FOW2 and FTF1, both encoding Zn(II)2Cys6-type transcriptional regulators [9,10,11,12]
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