(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) > cellular organisms: NE > Eukaryota: NE > Opisthokonta: NE > Fungi: NE > Dikarya: NE > Ascomycota: NE > saccharomyceta: NE > Pezizomycotina: NE > leotiomyceta: NE > sordariomyceta: NE > Sordariomycetes: NE > Hypocreomycetidae: NE > Hypocreales: NE > Nectriaceae: NE > Fusarium: NE > Fusarium oxysporum species complex: NE > Fusarium oxysporum: NE
Warning: This entry is a compilation of different species or line or strain with more than 90% amino acid identity. You can retrieve all strain data
(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) Fusarium oxysporum Fo5176: N, E.
Fusarium oxysporum f. sp. lycopersici 4287: N, E.
Fusarium oxysporum f. sp. cubense race 4: N, E.
Fusarium fujikuroi IMI 58289: N, E.
Fusarium oxysporum f. sp. cubense race 1: N, E.
Fusarium verticillioides 7600: N, E.
Fusarium oxysporum FOSC 3-a: N, E.
Fusarium oxysporum Fo47: N, E.
Fusarium oxysporum f. sp. lycopersici MN25: N, E.
Fusarium oxysporum f. sp. pisi HDV247: N, E.
Fusarium oxysporum f. sp. melonis 26406: N, E.
Fusarium oxysporum f. sp. raphani 54005: N, E.
Fusarium oxysporum f. sp. radicis-lycopersici 26381: N, E.
Fusarium oxysporum f. sp. conglutinans race 2 54008: N, E.
Fusarium oxysporum f. sp. cubense tropical race 4 54006: N, E.
Fusarium oxysporum f. sp. vasinfectum 25433: N, E.
Gibberella fujikuroi: N, E.
Fusarium fujikuroi: N, E.
LegendThis sequence has been compared to family alignement (MSA) red => minority aminoacid blue => majority aminoacid color intensity => conservation rate title => sequence position(MSA position)aminoacid rate Catalytic site Catalytic site in the MSA MYSLMSPAVLLGSLFFSFLAAANSSIPQVTLQGYGSFAGTNISKTLLGDN LPQPVNAWLGIDYAEQPVGDRRFRPLQSQPQSLKGLQNATKYRSVCLQDR MYPNPDEQDEACLNFNVFRTPGVPLSKKLPTLVWIHGGGFASFSGRDFDG ASFVASSADPVVVVTFNYRLNAFGFLPSKLFEREGLLNLGLQDQRFFLQF LQKHLSSFGGDPRQITLGGLSAGAHSTAFHYFHNYGSDKNKPLFARGILQ SGSATARSFPGPDYPRYKKDFAGLMKYINCSTDVDDNEQMGCLRSASTEK IREYSAKAYEDAKDQLNWPWQPSIGGPLIEKAGSKSEEEGTFHHLPIITT YTSDEGKYYTPGDLETNDDFVQFWHRISPGLNITDLALINELYPDPVAYP DSPWAGSPNSTQYNRISAAWSDMAYICMSRHTAVTTSRAGVPTWSLHFNT PDFPLVAQSWKGIPHASDAAYIWNDPHVAYPETARIYYRYINSFVLTGDP NKMRLDGTVEWPQYKAGENGNGYAKQLLVNPGNFTVVEEDRGRGRQCEFW NDIERAGRLYK
The fungus Fusarium fujikuroi causes "bakanae" disease of rice due to its ability to produce gibberellins (GAs), but it is also known for producing harmful mycotoxins. However, the genetic capacity for the whole arsenal of natural compounds and their role in the fungus' interaction with rice remained unknown. Here, we present a high-quality genome sequence of F. fujikuroi that was assembled into 12 scaffolds corresponding to the 12 chromosomes described for the fungus. We used the genome sequence along with ChIP-seq, transcriptome, proteome, and HPLC-FTMS-based metabolome analyses to identify the potential secondary metabolite biosynthetic gene clusters and to examine their regulation in response to nitrogen availability and plant signals. The results indicate that expression of most but not all gene clusters correlate with proteome and ChIP-seq data. Comparison of the F. fujikuroi genome to those of six other fusaria revealed that only a small number of gene clusters are conserved among these species, thus providing new insights into the divergence of secondary metabolism in the genus Fusarium. Noteworthy, GA biosynthetic genes are present in some related species, but GA biosynthesis is limited to F. fujikuroi, suggesting that this provides a selective advantage during infection of the preferred host plant rice. Among the genome sequences analyzed, one cluster that includes a polyketide synthase gene (PKS19) and another that includes a non-ribosomal peptide synthetase gene (NRPS31) are unique to F. fujikuroi. The metabolites derived from these clusters were identified by HPLC-FTMS-based analyses of engineered F. fujikuroi strains overexpressing cluster genes. In planta expression studies suggest a specific role for the PKS19-derived product during rice infection. Thus, our results indicate that combined comparative genomics and genome-wide experimental analyses identified novel genes and secondary metabolites that contribute to the evolutionary success of F. fujikuroi as a rice pathogen.
Title: A highly conserved effector in Fusarium oxysporum is required for full virulence on Arabidopsis Thatcher LF, Gardiner DM, Kazan K, Manners JM Ref: Mol Plant Microbe Interact, 25:180, 2012 : PubMed
Secreted-in-xylem (SIX) proteins of the vascular wilt pathogen Fusarium oxysporum f. sp. lycopersici are secreted during infection of tomato and function in virulence or avirulence. F. oxysporum formae speciales have specific host ranges but the roles of SIX proteins in diverse hosts are unknown. We identified homologs of F. oxysporum f. sp. lycopersici SIX1, SIX4, SIX8, and SIX9 in the genome of Arabidopsis infecting isolate Fo5176. A SIX4 homolog (termed Fo5176-SIX4) differed from that of F. oxysporum f. sp. lycopersici (Fol-SIX4) by only two amino acids, and its expression was induced during infection of Arabidopsis. Transgenic Arabidopsis plants constitutively expressing Fo5176-SIX4 had increased disease symptoms with Fo5176. Conversely, Fo5176-SIX4 gene knock-out mutants (Deltasix4) had significantly reduced virulence on Arabidopsis, and this was associated with reduced fungal biomass and host jasmonate-mediated gene expression, the latter known to be essential for host symptom development. Full virulence was restored by complementation of Deltasix4 mutants with either Fo5176-SIX4 or Fol-SIX4. Thus, Fo5176-SIX4 contributes quantitatively to virulence on Arabidopsis whereas, in tomato, Fol-SIX4 acts in host specificity as both an avirulence protein and a suppressor of other race-specific resistances. The strong sequence conservation for SIX4 in F. oxysporum f. sp. lycopersici and Fo5176 suggests a recent common origin.
Fusarium species are among the most important phytopathogenic and toxigenic fungi. To understand the molecular underpinnings of pathogenicity in the genus Fusarium, we compared the genomes of three phenotypically diverse species: Fusarium graminearum, Fusarium verticillioides and Fusarium oxysporum f. sp. lycopersici. Our analysis revealed lineage-specific (LS) genomic regions in F. oxysporum that include four entire chromosomes and account for more than one-quarter of the genome. LS regions are rich in transposons and genes with distinct evolutionary profiles but related to pathogenicity, indicative of horizontal acquisition. Experimentally, we demonstrate the transfer of two LS chromosomes between strains of F. oxysporum, converting a non-pathogenic strain into a pathogen. Transfer of LS chromosomes between otherwise genetically isolated strains explains the polyphyletic origin of host specificity and the emergence of new pathogenic lineages in F. oxysporum. These findings put the evolution of fungal pathogenicity into a new perspective.
Fusarium oxysporum (Fusarium vascular wilt) Cutinase FoCut5A