Pre_GI: SWBIT SVG BLASTP

Query: NC_010513:44886 Xylella fastidiosa M12 chromosome, complete genome

Lineage: Xylella fastidiosa; Xylella; Xanthomonadaceae; Xanthomonadales; Proteobacteria; Bacteria

General Information: Causal agent of citrus variegated chlorosis. This organism was first identified in 1993 as the causal agent of citrus variegated chlorosis, a disease that affects varieties of sweet oranges. This disease was first noticed in Brazil in 1987, and it greatly affects commercial orchards resulting in crop devastation worldwide. Other strains of this species cause a range of diseases in mulberry, pear, almond, elm, sycamore, oak, maple, pecan and coffee which collectively result in multimillion dollar devastation of economically important plants. The bacteria are transmitted from the gut of the insect vector (sharpshooter leafhopper) to the plant xylem (water conducting system) when the insect feeds. Xylella fastidiosa is similar to Xanthomonas campestris pv. campestris in that it produces a wide variety of pathogenic factors for colonization in a host-specific manner including a large number of fimbrial and afimbrial adhesins for attachment. It does not contain a type III secretion system, but possesses genes for a type II secretion system for export of exoenzymes that degrade the plant cell wall and allow the bacterium to colonize the plant xylem. The cell produces an exopolysaccharide that is similar to the xanthan gum produced by Xanthomonas campestris pv. campestris.

Subject: NC_003919:457482 Xanthomonas axonopodis pv. citri str. 306, complete genome

Lineage: Xanthomonas citri; Xanthomonas; Xanthomonadaceae; Xanthomonadales; Proteobacteria; Bacteria

General Information: This organism is the causal agent of citrus canker, a bacterial infection originating from southeast Asia which now occurs worldwide. Primarily a pathogen of plants in the Citrus genus, the disease is sometimes also found in other members of the Rutaceae. The bacterium survives in leaf, shoot and fruit lesions that develop during the spring, and which also cause secondary infections. During warm, wet weather in spring and early summer, the bacterium oozes out of overwintering lesions and infects new growth via the stomal pores or wounds. The bacterium may also survive for various periods of time in the soil or associated with other hosts.