The 5.67-megabase genome of the plant pathogen Agrobacterium tumefaciens C58 consists of a circular chromosome, a linear chromosome, and two plasmids. Extensive orthology and nucleotide colinearity between the genomes of A. tumefaciens and the plant symbiont Sinorhizobium meliloti suggest a recent evolutionary divergence. Their similarities include metabolic, transport, and regulatory systems that promote survival in the highly competitive rhizosphere; differences are apparent in their genome structure and virulence gene complement. Availability of the A. tumefaciens sequence will facilitate investigations into the molecular basis of pathogenesis and the evolutionary divergence of pathogenic and symbiotic lifestyles.

Genetic mapping showed that the rice blast avirulence gene AVR-Pita is tightly linked to a telomere on chromosome 3 in the plant pathogenic fungus Magnaporthe grisea . AVR-Pita corresponds in gene-for-gene fashion to the disease resistance ( R ) gene Pi-ta . Analysis of spontaneous avr-pita Ϫ mutants indicated that the gene is located in a telomeric 6.5-kb BglII restriction fragment. Cloning and DNA sequencing led to the identification of a candidate gene with features typical of metalloproteases. This gene is located entirely within the most distal 1.5 kb of the chromosome. When introduced into virulent rice pathogens, the cloned gene specifically confers avirulence toward rice cultivars that contain Pi-ta . Frequent spontaneous loss of AVR-Pita appears to be the result of its telomeric location. Diverse mutations in AVR-Pita , including point mutations, insertions, and deletions, permit the fungus to avoid triggering resistance responses mediated by Pi-ta . A point mutation in the protease consensus sequence abolishes the AVR-Pita avirulence function. INTRODUCTIONRice blast disease, caused by the fungus Magnaporthe grisea (Hebert) Barr (Rossman et al., 1990), remains one of the most important constraints to rice production worldwide, despite the availability of dozens of "major" disease resistance ( R ) genes, which are known as Pi genes (Yamada et al., 1976; Zeigler et al., 1994). Resistance mediated by Pi genes has not been durable, typically failing under field conditions soon after new cultivars are introduced to the field as new races, or pathotypes, of the pathogen appear with the ability to attack the previously resistant rice cultivars. Sasaki first distinguished differences in cultivar specificity between rice blast field isolates in 1922 (Yamada, 1985); since then, hundreds of pathogen races have been identified based on their infection spectra on differential rice cultivars. Recently, DNA fingerprinting analyses have shown that rice blast fungal populations are asexual and consist of dozens of families (discretely separable clonal lineages) having apparently predictable responses toward specific R genes (Levy et al., 1993; Zeigler et al., 1994). Lineage exclusion strategies are currently being tested as an aid for deploying R genes for genetic control of rice blast disease.The rice blast system is a classical gene-for-gene system (Flor, 1971) in which avirulence ( AVR ) genes in the pathogen show a functional correspondence with particular R genes in rice (Silué et al., 1992; Zeigler et al., 1994). AVR genes may encode pathogen molecules that are themselves recognized, directly or indirectly, by the corresponding R gene product, or they may encode enzymes involved in production of small molecule ligands that serve as recognition factors. Pathogen recognition triggers host resistance responses and stops infection. Field efficacy of any R gene thus depends on the biology of its associated AVR gene. Specifically, R gene efficacy depends on the nature of any function that an AVR gene may provide for th...

Rice blast disease is caused by a fungus that attacks all above-ground parts of the rice plant. In a study of the means by which the fungus attaches to the hydrophobic rice leaf surface, it was found that spores(conidia) of the rice blast fungus Magnaporthe grisea have a mechanism for immediate and persistent attachment to various surfaces, including Teflon. This attachment occurs at the spore apex and is blocked by the addition of the lectin concanavalin A. Microscopy of hydrated conidia shows that a spore tip mucilage that binds concanavalin A is expelled specifically from the conidial apex before germ tube emergence. Ultrastructural analysis of dry conidia shows a large periplasmic deposit, presumably spore tip mucilage, at the apex. The results indicate a novel mechanism for the attachment of phytopathogenic fungal spores to a plant surface.

We report a new fungal selectable marker that confers resistance to chlorimuron ethyl, a sulfonylurea herbicide. This gene as well as genes that confer resistance to hygromycin and bialaphos have been engineered to be compact and to eliminate sites for most common restriction enzymes. These three selectable markers have been used to construct a series of vectors for fungal transformation.