OutlineClick the species name for a description of the organism
Fungi of the Fusarium oxysporum species complex (FOSC) are ubiquitous soil and plant inhabiting microbes. As plant pathogens, FOSC strains can cause wilt and root rot diseases on over 120 plant species (Michielse and Rep, 2009). Many FOSC strains can infect plant roots without apparent effect or can even protect plants from subsequent infection (Alabouvette et al., 2009). FOSC isolates also have been identified as human pathogens causing localized or disseminated infections that may become life-threatening in neutropenic individuals (O'Donnell et al., 2004).
The F. oxysporum comparative genomes project has sought to make available genome sequence data for FOSC strains with a range of host specificities. The first genome made available in 2007 was from a tomato wilt strain FOL 4287 (NRRL 34936) which was used for comparative analysis with the genomes of F. graminearum and F. verticillioides. Results of this comparison led to the discovery of mobile supernumerary chromosomes in this strain of F. oxysporum f. sp. lycopersici (race 2 - VCG 0030) containing genes required for host specific infection and disease (Ma et al., 2010).
Eleven additional FOSC strains now have been sequenced. Two of these additional strains also infect tomato. MN25 (NRRL 54003) is a strain of F. oxysporum f. sp. lycopersici (race 3 - VCG 0033) from Manatee County, Florida (Gale et al., 2003). CL57 (NRRL 26381) is a tomato crown rot pathogen F. oxysporum f. sp. radicis-lycopersici (VCG 0094) from Collier County, Florida (Rosewich et al., 1999).
Two FOSC strains sequenced have specificity to crucifers. PHW808 (NRRL 54008) is a strain of F. oxysporum f. sp. conglutinans, race 2 (VCG 0101) from California that causes cabbage yellows disease. PHW815 (NRRL 54005) is a strain of F. oxysporum f. sp. raphani (VCG 0102) from France that causes radish wilt. Both strains cause wilt disease in Arabidopsis (Diener and Ausubel, 2005).
Fusarium wilt of banana can be an especially devastating disease of this crop (Fourie et al., 2011) caused by F. oxysporum f. sp. cubense. II5 (NRRL 54006) a strain of F. oxysporum f. sp. cubense tropical race 4 (VCG 01213) from Indonesia was sequenced. Strains of the fungus causing wilt disease on melon (F. oxysporum f. sp. melonis NRRL 26406), cotton (F. oxysporum f. sp. vasinfectum NRRL 25433) and pea (F. oxysporum f. sp. pisi NRRL 37622) also were sequenced.
F. oxysporum strain NRRL 32931, obtained from human blood, represents a distinct haplotype ST 128 (O'Donnell et al., 2004, 2009) and is closely related to FOSC 3-a/ST 333-a (O'Donnell et al., 2004). Pathogenic FOSC strains can cause localized necrotic diseases in immunocompetent individuals, including, for example, remarkable outbreaks of Fusarium keratitis among contact lens users (Chang et al., 2006) and may also cause life threatening disseminated infections in severely neutropenic patients (Boutati and Anaissie, 1997).
F. oxysporum strain Fo47 (NRRL 54002) is well-known for its biological control properties (Fravel et al., 2003). This strain was originally isolated from disease suppressive soils from the Chateaurenard region of France and demonstrated to colonize host roots and to be the biotic component of wilt disease suppression.
What follows is a summary table of the strains:
|NRRL #||Strain||forma specialis||Host|
|54003||MN25||lycopersici race 3||Lycopersicum|
|54008||PHW808||conglutinans, race 2||Brassica/Arabidopsis|
|54006||II5||cubense tropical race 4||Musa|
- Alabouvette,C., Olivain,C., Migheli,Q., and Steinberg,C. (2009) Microbiological control of soil-borne phytopathogenic fungi with special emphasis on wilt-inducing Fusarium oxysporum. New Phytologist 184: 529-544.
- Boutati,E.I., and Anaissie,E.J. (1997) Fusarium, a significant emerging pathogen in patients with hematologic malignancy: Ten years' experience at a cancer center and implications for management. Blood 90: 999-1008.
- Chang,D.C., Grant,G.B., O'Donnell,K., Wannemuehler,K.A., Noble-Wang,J., Rao,C.Y. et al. (2006) Multistate outbreak of Fusarium keratitis associated with use of a contact lens solution. JAMA 296: 953-963.
- Diener,A.C., and Ausubel,F.M. (2005) Resistance to Fusarium oxysporum 1, A dominant Arabidopsis disease-resistance gene, is not race specific. Genetics 171: 305-321.
- Fourie,G., Steenkamp,E.T., Ploetz,R.C., Gordon,T.R., and Viljoen,A. (2011) Current status of the taxonomic position of Fusarium oxysporum formae specialis cubense within the Fusarium oxysporum complex. Infection Genetics and Evolution 11: 533-542.
- Fravel,D., Olivain,C., and Alabouvette,C. (2003) Fusarium oxysporum and its biocontrol. New Phytologist 157: 493-502.
- Gale,L.R., Katan,T., and Kistler,H.C. (2003) The probable center of origin of Fusarium oxysporum f. sp. lycopersici VCG 0033. Plant Disease 87: 1433-1438.
- Ma,L.J., van der Does,H.C., Borkovich,K.A., Coleman,J.J., Daboussi,M.J., Di Pietro,A. et al. (2010) Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium. Nature 464: 367-373.
- Michielse,C.B., and Rep,M. (2009) Pathogen profile update: Fusarium oxysporum. Molecular Plant Pathology 10: 311-324.
- O'Donnell,K., Sutton,D.A., Rinaldi,M.G., Magnon,K.C., Cox,P.A., Revankar,S.G. et al. (2004) Genetic diversity of human pathogenic members of the Fusarium oxysporum complex inferred from multilocus DNA sequence data and amplified fragment length polymorphism analyses: Evidence for the recent dispersion of a geographically widespread clonal lineage and nosocomial origin. Journal of Clinical Microbiology 42: 5109-5120.
- O'Donnell, K., Gueidan, C., Sink, S., Johnston, P.R., Crous, P.W., Glenn, A., Riley, R., Zitomer, N.C., Colyer, P., Waalwijk, C., et al. (2009) A two-locus DNA sequence database for typing plant and human pathogens within the Fusarium oxysporum species complex. Fungal Genet Biol 46: 936-948.
- Rosewich,U.L., Pettway,R.E., Katan,T., and Kistler,H.C. (1999) Population genetic analysis corroborates dispersal of Fusarium oxysporum f. sp radicis-lycopersici from Florida to Europe. Phytopathology 89: 623-630.
Fusarium graminearum is the causal agent of head blight (scab) of wheat and barley, a plant disease with great impact on U.S. agriculture and society during the past decade. Approximately $3 billion were lost to U. S. agriculture during wheat scab epidemics in the 1990s, resulting in devastating effects on farm communities in the upper Midwest and elsewhere (McMullen et al., 1997; Windels, 2000). Moreover, the disease is becoming a threat to the world's food supply due to recent head blight outbreaks in Asia, Canada, Europe and South America (Dubin et al., 1997). The fungus also infects and causes disease on corn and rice (Webster and Gunnell, 1992; White, 1999). The pathogen poses a two-fold threat: first, infested cereals are significantly reduced in seed quality and yield, and secondly, scabby grain is contaminated with trichothecene and estrogenic mycotoxins, making it unsuitable for food or feed (McMullen et al., 1997). As a food safety issue, trichothecene toxins such as "vomitoxin" (deoxynivalenol) pose a serious hazard to human and animal health because these sesquiterpenoids are potent inhibitors of eukaryotic protein biosynthesis. Vomitoxin causes weight loss and feeding refusal in non-ruminant livestock, and human ingestion of grain contaminated with F. graminearum has been associated with alimentary toxic aleukia as well as illness characterized by nausea, vomiting, anorexia, and convulsions (Murphy and Armstrong, 1995). Trichothecenes also are powerful modulators of human immune function and may promote neoplasms, cause autoimmune disease, or have long-term effects on resistance to infectious disease by altering immune response (Berek et al., 2001; Lindsay, 1997).
Sequenced strain information: The strain chosen for sequencing by the International Gibberella zeae Genomics Consortium (IGGR) was PH-1 (NRRL 31084). Fusarium graminearum is the predominant FHB species causing scab of wheat and barley in North America and Europe and is distributed worldwide (O'Donnell et al., 2000, 2004). Isolated in Michigan, PH-1 is highly fertile (Trail and Common, 2000), produces trichothecenes and zearalenone , sporulates abundantly in pure culture and is highly pathogenic to wheat and barley. The strain can be readily transformed and is closely related to strain GZ3639 (NRRL 29169) that has been studied for trichothecene biosynthesis (Brown et al., 2001) and strain 00-676 (NRRL 34097) used as one parent with PH-1 for the genetic map (Gale et al., 2005).References
- Batzoglou, S., D. B. Jaffe, K. Stanley, J. Butler, S. Gnerre, E. Mauceli, B. Berger, J. P. Mesirov, and E. S. Lander. 2002. ARACHNE: a whole-genome shotgun assembler. Genome Res 12: 177-89.
- Berek, L., I. B. Petri, A. A. Mesterhazy, J. Teren, and J. Molnar. 2001. Effects of mycotoxins on human immune functions in vitro. Toxicol. In Vitro 15:25-30.
- Brown, D. W., S. P. McCormick, N. J. Alexander, R. H. Proctor, and A. E. Desjardins. 2001. A genetic and biochemical approach to study trichothecene diversity in Fusarium sporotrichioides and Fusarium graminearum. Fungal Genet.Biol. 32:121-133.
- Dubin, H. J., L. Gilchrist, L. Reeves, and A. McNab. 1997. Fusarium Head Blight: Global Status and Prospects. CIMMYT, Mexico City.
- Jaffe, D. B., J. Butler, S. Gnerre, E. Mauceli, K. Lindblad-Toh, J. P. Mesirov, M. C. Zody, and E. S. Lander. 2003. Whole-genome sequence assembly for mammalian genomes: Arachne 2. Genome Res 13: 91-6.
- Lindsay, J. A. 1997. Chronic sequelae of foodborne disease. Emerg.Infect.Dis. 3:443-452.
- McMullen, M., R. Jones, and D. Gallenberg. 1997. Scab of wheat and barley: A re-emerging disease of devastating impact. Plant Dis. 81:1340-1348.
- Murphy, M. and D. Armstrong. 1995. Fusariosis in patients with neoplastic disease. Infect.Med. 12:66-67.
- O'Donnell, K., H. C. Kistler, B. K. Tacke, and H. H. Casper. 2000. Gene genealogies reveal global phylogeographic structure and reproductive isolation among lineages of Fusarium graminearum, the fungus causing wheat scab. Proc.Natl.Acad.Sci.U.S.A. 97:7905-7910.
- Rostker, B. 2000. Closeout Report, Biological Warfare Investigation, Gulf War Illnesses.
- Trail, F. and R. Common. 2000. Perithecial development by Gibberella zeae: a light microscopy study. Mycologia 92:130-138.
- Wannemacher, R. W. and S. L. Wiener. 1989. Trichothecene mycotoxins, p. 655-676. In: F. R. Sidell, E. T. Takafuji, and D. R. Franz (eds.), Medical Aspects of Chemical and Biological Warfare. Office of the Surgeon General at TMM Publications, Washington, DC.
- Ward, T.J., J.P. Bielawski, H.C. Kistler, E. Sullivan, and K. O'Donnell. 2002. Ancestral polymorphism and adaptive evolution in the trichothecene gene cluster of phytopathogenic Fusarium. Proc. Natl. Acad. Sci. U.S.A. 99:9278-9283.
- Webster, R. K. and P. S. Gunnell. 1992. Compendium of Rice Diseases. APS Press, The American Phytopathological Society, St. Paul, MN.
- White, D. G. 1999. Compendium of Corn Diseases. APS Press, The American Phytopathological Society, St. Paul, MN.
- Windels, C. E. 2000. Economic and social impacts of Fusarium head blight: Changing farms and rural communities in the Northern Great Plains. Phytopathology 90:17-21.
Fusarium verticillioides is the causal agent of kernel and ear rot of maize. This destructive disease occurs virtually everywhere that maize is grown worldwide. In years with high temperatures, drought, and heavy insect damage, the disease can significantly diminish crop quality.
The most significant economic impact of F. verticillioides is its ability to produce fumonisin mycotoxins. Various diseases caused by fumonisins have been reported in animals, such as liver and kidney cancer as well as neural tube defects in rodents (Howard et al. 2001, Seefelder et al. 2003), leukoencephalomalacia in equines (Wilson et al. 1992), and pulmonary edema in pigs (Kriek et al. 1981). More importantly, epidemiological correlations have been established between human esophageal cancer and the consumption of fumonisin-contaminated maize in some regions of the world where maize is a dietary staple. In addition, fumonisins have been reported to be a potential cause of neural tube defects in humans (Seefelder et al. 2003). Due to potential health risks, guidelines for fumonisin levels in food have been established by the US FDA and by other government agencies worldwide (FDA/CFSAN, 2001). In 2003, fumonisin B1, the fumonisin produced most abundantly by F. verticillioides, was added to the California Proposition 65 List of Substances Known to Cause Cancer.
Sequenced strain information: Strain 7600 (FRC M3125=NRRL 20956), which has been used extensively in molecular and pathological studies, was selected for the genome project. This strain is available at FGSC, NCAUR-ARS-USDA and the Fusarium Research Center at Penn State. The genome size is estimated to be 46 Mb with 12 chromosomes.References
- Howard, P. C., R. M. Eppley, M. E. Stack, A. Warbritton, K. A. Voss, R. J. Lorentzen, R. M. Kovach, and T. J. Bucci. 2001. Fumonisin B1 carcinogenicity in a two-year feeding study using F344 rats and B6C3F1 mice. Environmental Health Perspectives 109 S2: 277-282.
- Kriek, N. P. J., T. S. Kellerman, and W. F. O. Marasas. 1981. A comparative study of the toxicity of Fusarium verticillioides (= F. moniliforme) to horses, primates, pigs, sheep and rats. Ondersterpoort Journal of Veterinary Research 48: 129-131.
- Seefelder, W., H.-U. Humpf, G. Schwerdt, R. Freudinger, and M. Gekle. 2003. Induction of apoptosis in cultured human proximal tubule cells by fumonisins and fumonisin metabolites. Toxicol. Appl. Pharmacol. 192: 146-153.
- Wilson, T. M., P. F. Ross, D. L. Owens, L. G. Rice, S. A. Green, S. J. Jenkins, and H. A. Nelson. 1992. Experimental reproduction of ELEM - a study to determine the minimum toxic dose in ponies. Mycopathologia: 115-120.