Who are we?
The Magnaporthe grisea genome project is a partnership between the International Rice Blast Genome Consortium, and the Broad Institute. The project is facilitated by an Advisory Board made up of members of the rice blast research community.
Ralph Dean, head of the International Rice Blast Genome Consortium, is the Director of the Fungal Genomics Laboratory and the Center for Integrated Fungal Research at NC State University. The Center is located on Centennial Campus adjacent to the Genome Research Laboratory and the Bioinformatics Research Center.
Collaborators for the project include:
- Department of Plant Pathology, North Carolina State University, Raleigh, NC 27695, USA
Department of Plant Pathology and Physiology, Clemson University, Clemson, SC 29634, USA
- H. Zhu
- B. Blackmon
A primary system studied in the Fungal Genomics laboratory is the interaction between rice and the rice blast fungus, Magnaporthe grisea, a major threat to food security worldwide. The goal is to perform a comprehensive molecular dissection of the mechanisms regulating early events of the host-pathogen recognition process, including the induction of a specialized infection cell, the appressorium, as well as host response genes.
The Eli and Edythe L. Broad Institute is a partnership among MIT, Harvard and affiliated hospitals and the Whitehead Institute for Biomedical Research. Its mission is to create the tools for genomic medicine and make them freely available to the world and to pioneer their application to the study and treatment of disease.
Questions about the project should be directed to email@example.com, firstname.lastname@example.org.
What is Magnaporthe grisea?
Magnaporthe grisea, the causal agent of rice blast disease, is one of the most devasting threats to food security worldwide. Conservatively, each year enough rice is destroyed by rice blast disease to feed 60 million people (Zeigler et al. 1994). Indeed, the Centers for Disease Control and Prevention has recently recognized and listed rice blast as a significant biological weapon. No part of the world is now safe from this disease. It was long thought of as being confirned to developing nations, but over the past decade it has emerged as a serious problem in the United States. A major epidemic occurred in the Southern US following the widespead introduction of the susceptible cultivar Newbonnet (Marchetti 1994).
The impact of this fungus is beginning to be felt in other ways. Certain strains are able to attack other domesticated grasses, including barley, wheat, pearl millet and turf-grass. Limited outbreaks on wheat have been reported in South America (Valent and Chumley 1994). Widespread devastation of golf courses, particularly in the Midwest, where it has been attacking cool season grasses, is of particular concern (Landschoot and Hoyland 1992).
|Cross-section of appressorium of wild Magnaporthe grisea.|
Like many foliar plant pathogens, M. grisea is well adapted to attack and penetrate its host. All aerial parts of the plant are subject to invasion, but losses are most devastating when the panicle or node at the base of the panicle is infested and killed resulting in loss of grain set (Ou 1985). The infection process is similar to that of many other fungal pathogens and is mediated by the formation of a specialized infection cell, the appressorium (Emmet and Parberry 1975). Although much has been learned, it remains largely a mystery how the emerging germ tube recognizes it is on a suitable surface and sets in motion a series of elaborate development steps that culminate in infection (Dean 1997).
Management of rice blast disease is most precarious (Bonman and MacKill 1988). While in the past, control was mainly through use of expensive and potentially hazardous chemicals (when affordable) the focus has shifted, as it has for most diseases, to more environmentally friendly and potentially less expensive approaches, principally mediated through host resistance. The rice blast genome appears to be quite unstable and in some instances new races appear relatively quickly. A key to developing effective and durable resistance is through a comprehensive understanding of the host-pathogen interaction, which in turn requires a thorough understanding of both the host and the pathogen.
Magnaporthe grisea is an excellent model organism for studying fungal phytopathogenicity and host-parasite interactions. M. grisea is a haploid, filamentous Ascomycete with a relatively small genome of ~40 Mb contained in 7 chromosomes (Talbot et al. 1993; Orbach 1996). The majority of fungal pathogens belong to this taxonomic class or exist as related asexual forms (Agrios 1997). M. grisea is also closely related to the non-pathogen Neurospora crassa, a leading model organism for the study of eukaryotic genetics and biology (Taylor et al. 1993). Unlike many phytopathogenic fungi such as mildews and rusts, the rice blast fungus can be cultured on defined media, facilitating biochemical and molecular analyses. Significantly, early stages of the infection process including germination, appressorium formation and penetration can be studied ex planta (Hamer et al. 1988; Bourett and Howard 1990; Howard and Valent 1996; Dean 1997).
We were funded for this project under joint USDA/NSF grants to attempt 7x sequence coverage comprising paired end reads from plasmids, Fosmids and BACs. Our strategy involves Whole Genome Shotgun (WGS) sequencing, in which sequence from the entire genome is generated and reassembled. Our long-term goal is to obtain the complete and finished DNA sequence of the M. grisea genome. To this end, members of the M. grisea research community have cooperatively planned and produced a number of critical resources needed to generate this sequence, ensure its accuracy, and maximize its utility. Our immediate goal is to make use of these resources to rapidly produce a highly accurate whole genome-based analysis of this organism and the disease it causes. The rapid availability of this sequence in an annotated form will immediately promote discovery of genes and potential anti-fungal targets, permit reconstruction of pathways, provide sequence-anchored clone paths for use in genetic and functional studies, and enable comparative genomic approaches to analysis.
The International Rice Blast Genome Consortium has agreed to use the rice-infecting strain 70-15 as the seminal isolate for genome sequencing. This isolate was developed by numerous back crosses to the wild isolate Guy 11 (Leung et al. 1988; Chao and Ellingboe 1991). Strain 70-15 (Mat1-1) is pathogenic on rice and is fully fertile (acts as both male and female). Crosses can be made with its sib strain 70-6 and many other strains carrying Mat1-2. Numerous resources have been generated for this isolate, including cDNA, cosmid and BAC libraries, many of which are distributed among the Magnaporthe community.
Our specific aims are as follows:
- Generate and assemble sequence reads yielding 7X coverage of the Magnaporthe grisea genome through whole genome shotgun sequencing.
- Generate and incorporate BAC and Fosmid end sequences into the genome assembly to provide a paired-end of average every 2 kb.
- Integrate the genome sequence with existing physical and genetic map information.
- Perform automated annotation of the sequence assembly.
- Distribute the sequence assembly and results of our annotation and analysis through a freely accessible, public web server and by deposition of the sequence assembly in GenBank.
|Release 1||Sequence assembly release|
|Release 2||Automated annotation, preliminary genome analysis and integration with genetic map|
|Release 5||Automated annotation, preliminary genome analysis and integration with genetic map|
|Release 6||Automated annotation, preliminary genome analysis and integration with genetic map|
We have modified our Gene Naming guidelines to be less conservative, resulting in changes to the names of 3605 genes. None of the underlying gene structures have been modified, nor have contig sequences have been modified from release 2.1. See Release 2.2 Details for more information. This is in addition to our recent improvements to our gene calling software, which this resulted in 17 genes being modified and 3 genes being added to our putative gene set. Our gene set contains 11,109 genes. See Release 2.1 Details for more information.
- Agrios, G.N. 1997. Plant Pathology. Academic Press, San Diego, CA.
- Bonman, J.M. and D.J. MacKill. 1988. Durable resistance to rice blast disease. Oryza 25: 103-110.
- Bourett, T.M. and R.J. Howard. 1990. In vitro development of penetration structures in the rice blast fungus Magnaporthe grisea. Can. J. Bot. 68: 329-342.
- Chao, C.C.T. and A.H. Ellingboe. 1991. Selection for mating competence in Magnaporthe grisea pathogenic to rice. Can. J. Bot. 69: 2130-2134.
- Dean, R.A. 1997. Signal pathways and appressorium morphogenesis. Annu. Rev. Phytopathol. 35: 211-34.
- Emmet, R.W. and D.G. Parberry. 1975. Appressoria. Ann. Rev. Phytopathol. 13: 147-167.
- Hamer, J.E., R.J. Howard, F.G. Chumley, and B. Valent. 1988. A mechanism for surface attachment in spores of a plant pathogenic fungus. Science 239: 288-290.
- Howard, R.J. and B. Valent. 1996. Breaking and entering: host penetration by the fungal rice blast pathogen Magnaporthe grisea. Ann. Rev. Microbiol. 50: 491-512.
- Landschoot, P.J. and B.F. Hoyland, 1992. Gray leaf spot of perrenial ryegrass turf in Pennsylvania. Plant Disease 76: 1280-1282.
- Leung, H., S. Borromeo. M.A. Bernardo, and J.L. Notteghem. 1988. Genetic analysis of virulence in the rice blast fungus Magnaporthe grisea. Phytopathol. 78: 1227-1233.
- Marchetti, M.A. 1994. Race-specific and rate-reducing resistance to rice blast in US rice cultivars. In Rice Blast Disease (ed. R.S. Zeigler, S.A. Leong, and P.S. Teng), pp. 231-244. Cab International, Wallingford.
- Orbach, M.J. 1994. A cosmid with a HyR marker for fungal library construction and screening. Gene 150: 159-162.
- Orbach, M.J., F.G. Chumley, and B. Valent. 1996. Electrophoretic karyotypes of Magnaporthe grisea pathogens of diverse grasses. Molec. Plant-Microbe Interactions 9: 261-271.
- Ou, S.H. 1985. Rice Diseases, pp. 109-200. Commonwealth Mycological Institute, United Kingdom.
- Talbot, N.J., Y.P. Salch, M. Ma, and J.E. Hamer. 1993. Karyotypic variation with clonal lineages of the rice blast fungus, Magnaporthe grisea. Appl. and Env. Micro. 59: 585-593.
- Taylor, J.W., B.H. Bowman, M.L. Berbee, and T.J. White. 1993. Fungal Model Organisms: Phylogenetics of Saccharomyces, Aspergillus, and Neurospora. Syst. Biol. 42: 440-457.
- Valent, B. and F.G. Chumley. 1994. Avirulence genes and mechanisms of genetic instability in the rice blast fungus. In Rice Blast Disease (ed. R.S. Zeigler, S.A. Leong, and P.S. Teng), pp. 111-134. University Press, Cambridge.
- Zeigler, R.S., S.A. Leong, and P.S. Teng, 1994. Rice Blast Disease. In Rice Blast Disease, pp. 1-626. Cab International, Wallingford.
Electron micrograph image used with permission, from the Annual Review of Microbiology, Volume 50 © 1996 by Annual Reviews www.AnnualReviews.org