New Outbreaks of Bacterial Wilt of Dry Bean in Nebraska Observed from Field Infections

Bacterial wilt caused by Curtobacterium flaccumfaciens pv. flaccumfaciens was one of the more problematic diseases of dry bean (Phaseolus vulgaris L.) throughout the irrigated High Plains (Colorado, Nebraska, and Wyoming) in the 1960s and early 1970s, but has not been observed since that time. However, in August of 2003, plants exhibiting wilting and irregular, interveinal necrotic foliar lesions surrounded by a bright yellow border were found in three dry bean fields (market class Great Northern) in Scotts Bluff County, Nebraska. During 2004, plants exhibiting identical symptoms were additionally found occurring in more than 40 dry bean fields in western Nebraska. Affected fields were planted with dry bean from multiple market classes and seed sources, including yellow bean, Great Northern bean, and pinto bean, and incidence varied from trace levels to 80 to 90%. Isolations were made from leaf and stem tissues and seeds collected after harvest from infected plants, and all yielded slow-growing, creamy yellow or orange, fluidal colonies on nutrient broth-yeast extract medium. The bacterium was identified as C. flaccumfaciens pv. flaccumfaciens based on cell morphology (coryneform-shaped motile rods), positive Gram stain and KOH reactions, fatty acid profiles, and BIOLOG (Hayward, CA) identifications. Great Northern (cv. Orion) plants were inoculated by bacterial suspensions (5 × 107 CFU/ml) injected into leaf axils adjacent to the first fully expanded trifoliolate and were incubated in the greenhouse under ambient conditions fluctuating between 24 and 35°C. Wilting symptoms developed 7 days after inoculation with foliar necrosis and yellowing symptoms appearing after 24 days. Identical bacterial colonies were reisolated from inoculated tissues, completing Koch\u27s postulates. Although recent reports of wilt have been made in North Dakota (2) and western Canada (1) in 1995 and 2002, respectively, they were based only on the presence of discolored seeds observed in dockage from processing plants after harvest. To our knowledge, this report represents the first widespread observations of bacterial wilt from field infections in Nebraska in more than 30 years

Registration of Common Bacterial Blight, Rust and Bean Common Mosaic Resistant Great Northern Common Bean Germplasm Line ABC-Weihing

Great northern common bean (Phaseolus vulgaris L.) germplasm line ABC-Weihing (Reg. No. GP-246, PI 647964) was developed by the University of Nebraska Agricultural Research Division in cooperation with USDA-ARS and released in 2006. This line, tested as NE1-05-4, was bred specifically for enhanced resistance to common bacterial blight (CBB), a major seed borne disease of common bean caused by the bacterium Xanthomonas campestris pv. phaseoli (Smith) Dye (Xcp). ABC-Weihing is a great northern BC5F3:6 line obtained from five backcrosses (‘Weihing’*5//‘Chase’/XAN 159). The first cross was made in spring 1997. Only BCnF1 plants resistant to Xcp isolates Dominican Republic DR-7 and Nebraska SC4A, as determined by multiple needle leaf inoculation tests in the greenhouse, were used for successive backcrossing. In addition to phenotypic selection for CBB resistance, marker-assisted selection for the resistant QTLlinked marker SU91 was conducted in the BC1F1, BC2F1, and ABC-Weihing. When inoculated with Nebraska Xcp strains in the field, ABC-Weihing exhibited resistance in both 2005 and 2006. ABC-Weihing has Ur-3 and Ur-6 genes for resistance to common bean rust and carries the single dominant hypersensitive I gene that provides resistance to all non-necrotic strains of the Bean common mosaic virus (BCMV). ABC-Weihing has bright white seed, blooms 45 d after planting, and is a midseason bean maturing 92 d after planting

Reclassification of Subspecies of \u3ci\u3eAcidovorax avenae\u3c/i\u3e as \u3ci\u3eA. Avenae\u3c/i\u3e (Manns 1905) emend., \u3ci\u3eA. cattleyae \u3c/i\u3e (Pavarino, 1911)comb.nov., \u3ci\u3eA. citrulli\u3c/i\u3e Schaad et al.,1978)comb.nov., and proposal of \u3ci\u3eA. oryzae \u3c/i\u3esp. nov.

The bacterium Acidovorax avenae causes disease in a wide range of economically important monocotyledonous and dicotyledonous plants, including corn, rice, watermelon, anthurium, and orchids.Genotypic and phenotypic relatedness among strains of phytopathogenic A. avenae sub sp. avenae, A. avenae sub sp. citrulli, A. avenae subsp. cattleyae and A. konjaci, as well as all other Acidovorax species, including A. facilis, the type strain of Acidovorax, was determined.The16s rDNA sequencing confirmed previous studies showing the environmental species to be very distant from the phytopathogenic species. DNA/DNA reassociation assays on the different strains of A. avenae revealed four(A, B, C, and D) distinct genotypes. Taxon A included six A. avenae subsp. avenaestrains from corn that had a mean reciprocal similarity of 81%; taxon B included six A. avenae sub sp. avenae strains from rice that had a mean reciprocal similarity of 97%; taxon C contained 11 A. avenae sub sp. citrulli strains from cucurbits (cantaloupe, watermelon, and pumpkin) that had a mean reciprocal similarity of 88%, and taxon D contained four A. avenae sub sp. cattleyae strains from orchids that had a mean similarity of 98%

Adaptations of Avian Flu Virus Are a Cause for Concern

We are in the midst of a revolutionary period in the life sciences. Technological capabilities have dramatically expanded, we have a much improved understanding of the complex biology of selected microorganisms, and we have a much improved ability to manipulate microbial genomes. With this has come unprecedented potential for better control of infectious diseases and significant societal benefit. However, there is also a growing risk that the same science will be deliberately misused and that the consequences could be catastrophic. Efforts to describe or define life-sciences research of particular concern have focused on the possibility that knowledge or products derived from such research, or new technologies, could be directly misapplied with a sufficiently broad scope to affect national or global security. Research that might greatly enhance the harm caused by microbial pathogens has been of special concern (1–3). Until now, these efforts have suffered from a lack of specificity and a paucity of concrete examples of “dual use research of concern” (3). Dual use is defined as research that could be used for good or bad purposes. We are now confronted by a potent, real-world example

Ligand-Induced Movements of Inner Transmembrane Helices of Glut1 Revealed by Chemical Cross-Linking of Di-Cysteine Mutants

The relative orientation and proximity of the pseudo-symmetrical inner transmembrane helical pairs 5/8 and 2/11 of Glut1 were analyzed by chemical cross-linking of di-cysteine mutants. Thirteen functional di-cysteine mutants were created from a C-less Glut1 reporter construct containing cysteine substitutions in helices 5 and 8 or helices 2 and 11. The mutants were expressed in Xenopus oocytes and the sensitivity of each mutant to intramolecular cross-linking by two homobifunctional thiol-specific reagents was ascertained by protease cleavage followed by immunoblot analysis. Five of 9 mutants with cysteine residues predicted to lie in close proximity to each other were susceptible to cross-linking by one or both reagents. None of 4 mutants with cysteine substitutions predicted to lie on opposite faces of their respective helices was susceptible to cross-linking. Additionally, the cross-linking of a di-cysteine pair (A70C/M420C, helices 2/11) predicted to lie near the exoplasmic face of the membrane was stimulated by ethylidene glucose, a non-transported glucose analog that preferentially binds to the exofacial substrate-binding site, suggesting that the binding of this ligand stimulates the closure of helices at the exoplasmic face of the membrane. In contrast, the cross-linking of a second di-cysteine pair (T158C/L325, helices 5/8), predicted to lie near the cytoplasmic face of the membrane, was stimulated by cytochalasin B, a glucose transport inhibitor that competitively inhibits substrate efflux, suggesting that this compound recruits the transporter to a conformational state in which closure of inner helices occurs at the cytoplasmic face of the membrane. This observation provides a structural explanation for the competitive inhibition of substrate efflux by cytochalasin B. These data indicate that the binding of competitive inhibitors of glucose efflux or influx induce occluded states in the transporter in which substrate is excluded from the exofacial or endofacial binding site