Query: NC_012416:852000 Wolbachia sp. wRi, complete genome Lineage: Wolbachia; Wolbachia; Anaplasmataceae; Rickettsiales; Proteobacteria; Bacteria General Information: Endosymbiont. Obligate intracellular bacterium infects around 20% of all insect species. Naturally infects Drosophila simulans and induces almost complete cytoplasmic incompatibility in its host. Wolbachia sp. subsp. Drosophila simulans (strain wRi) is an intracellular proteobacterium that infect insects as well as isopods, spiders, scorpions, mites, and filarial nematodes. It is maternally inherited and induces reproductive alterations of insect populations by male killing, feminization, parthenogenesis, or cytoplasmic incompatibility. In insect populations, Wolbachia sp. induce reproductive manipulations to enhance their own spreading. The most frequently observed reproductive abnormality is cytoplasmic incompatibility, where uninfected females are unable to produce offspring with infected males, whereas infected females can produce offspring with both infected and uninfected males, thus creating a reproductive advantage for infected females. Other spectacular effects of Wolbachia sp. infections are male embryo killing, feminization, and parthenogenesis induction.
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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.