Pre_GI: SWBIT SVG BLASTN

Query: NC_008358:2808299 Hyphomonas neptunium ATCC 15444, complete genome

Lineage: Hyphomonas neptunium; Hyphomonas; Hyphomonadaceae; Rhodobacterales; Proteobacteria; Bacteria

General Information: Marine member of dimorphic prosthecate bacteria. This organism is also known as Hyphomicrobium neptunium. It has a biphasic life style, which consists of a motile phase of flagellated swarmer cells, and a cessile phase in which a long prosthecate is produced at one end of the bacteria through which budding cells emerge. Newly budded cells in turn produce flagella and go through a motile phase and the cycle continues. These organisms can colonize the surfaces of marine environments which enables additional species to colonize at later stages. This organism may be of use in treatment of water as they attach to a solid surface and are capable of degradation of a number of pollutants including aromatic hydrocarbons, dimethyl sulfoxide and methyl chloride.

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Subject: NC_005956:1402500 Bartonella henselae str. Houston-1, complete genome

Lineage: Bartonella henselae; Bartonella; Bartonellaceae; Rhizobiales; Proteobacteria; Bacteria

General Information: Bartonella henselae str. Houston-1 (ATCC 49882) was isolated from human blood in Houston Texas. Causative agent of cat scratch fever. This group of alpha proteobacteria are unique among pathogens in that they cause angiogenic lesions. This organism was identified as the causative agent of cat scratch fever, a disease found commonly in children or in immunocompromised adults. The proliferation of the vascular endothelium (bacillary angiomatosis) is characterisitic of Bartonella infection and results in multiplication of the bacterium's host cells. Infected macrophages are stimulated to release vascular endothelial growth factor (VEGF) and interleukin 1 beta, both of which promote angiogenesis. Endothelial cells are also stimulated to grow and divide by direct contact with bacterial cells. In addition, programmed cell death (apoptosis) of endothelial cells is inhibited, combatting a common mechanism eukaryotic cells use to deal with bacterial infection. Other pathogenicity factors include pili and outer membrane adhesins for attachment to host cells.