Query: NC_017259:25400 Buchnera aphidicola str. Ua (Uroleucon ambrosiae) chromosome, Lineage: Buchnera aphidicola; Buchnera; Enterobacteriaceae; Enterobacteriales; Proteobacteria; Bacteria General Information: It is believed that the Buchnera provide the essential nutrients the host lacks. Besides a nutritional co-dependence, due to a co-existence of millions of years, Buchnera have lost the ability to produce cell surface components such as lipopolysaccharides. This makes for an obligate endosymbiont relationship between host and Buchnera. Buchnera are prokaryotic cells which belong to the gamma-Proteobacteria, closely related to the Enterobacteriaceae family. Phylogenetic studies using 16S rRNA indicate that the symbiotic relationship was established around 200-250 million years ago. Since Buchnera are closely related to Escherichia coli and Haemophilus influenzae, comparative genomic studies can shed light on the evolutionary mechanisms of intracellular endosymbiosis as well as the different underlying molecular basis between organisms with parasitic behavior and symbionts.
- Sequence; - BLASTP hit: hover for score (Low score = Light, High score = Dark); - hypothetical protein; - cds: hover for description
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.