Pre_GI: SWBIT SVG BLASTN

Query: NC_016047:261304 Bacillus subtilis subsp. spizizenii TU-B-10 chromosome, complete

Lineage: Bacillus subtilis; Bacillus; Bacillaceae; Bacillales; Firmicutes; Bacteria

General Information: This organism was one of the first bacteria studied, and was named Vibrio subtilis in 1835 and renamed Bacillus subtilis in 1872. It is one of the most well characterized bacterial organisms, and is a model system for cell differentiation and development. This soil bacterium can divide asymmetrically, producing an endospore that is resistant to environmental factors such as heat, acid, and salt, and which can persist in the environment for long periods of time. The endospore is formed at times of nutritional stress, allowing the organism to persist in the environment until conditions become favorable. Prior to the decision to produce the spore the bacterium might become motile, through the production of flagella, and also take up DNA from the environment through the competence system. The sporulation process is complex and involves the coordinated regulation of hundreds of genes in the genome. This initial step results in the coordinated asymmetric cellular division and endospore formation through multiple stages that produces a single spore from the mother cell.

Subject: NC_008710:621822 Borrelia turicatae 91E135, complete genome

Lineage: Borrelia turicatae; Borrelia; Spirochaetaceae; Spirochaetales; Spirochaetes; Bacteria

General Information: This strain was isolated in the USA from the soft tick Ornithodoros turicatae. Borrelia turicatae is the causative agent of tick-borne relapsing fever in the southwestern USA. Ticks become infected with Borrelia while feeding on an infected mammal, usually a rodent or squirrel. Borrelia then multiplies rapidly, causing a generalized infection throughout the tick. While feeding, the tick passes the spirochete into a mammalian host through its infectious saliva. Relapsing fever is characterized by period of chills, fever, headache, and malaise, followed by an asymptomatic, followed by another episode of symptoms. The cycle of relapsing is due to changes in the surface proteins of Borrelia, which allow it to avoid detection and removal by the host immune system. This antigenic variation is the result of homologous recombination of silent proteins into an expressed locus, causing partial or complete replacement of one serotype with another. These plasmids carry genes involved in antigenic variation and pathogenicity.