Effector and immunity pairs must have evolved in tandem with a cognate immunity protein for each effector. cholerae: auxiliary cluster 1, auxiliary cluster 2 and a large cluster, each harbouring an effector-immunity pair: tseL & tsiV1, vasX & tsiV2 and vgrG3 & tsiV3, respectively. Three distinct genetic loci across two chromosomes encode the T6SS in V. These effectors are toxic unless inhibited by cognate immunity proteins in the attacked bacterium. Contraction of the T6SS outer sheath ejects an inner tube consisting of polymerised Hcp proteins, capped with effector proteins, into adjacent bacteria. The T6SS is a bacterial nanomachine embedded in the envelope of gram-negative bacteria that mediates contact-dependent translocation of effector toxins into neighbouring cells 2. cholerae virulence factor, the type-six secretion system (T6SS) 2. The generation of a high-resolution genomic sequence allowed us to track the evolution of one V. A preserved intestine from an 1849 cholera victim belonging to the Mütter Museum collection in Philadelphia offers unprecedented insights into 2nd pandemic V. As a result, DNA sequences are available principally from the 6th pandemic (classical biotype strains, 1899–1923) and the ongoing 7th pandemic (El Tor biotype strains, 1961–today). Therefore, historical specimens for DNA extraction are rare.
cholerae colonises soft tissues and is noninvasive.
Historical strains were not isolated until the germ theory became accepted in the late 1800s. Understanding how these O1 pandemic strains evolved is hampered by the absence of available strains. Throughout modern history, seven cholera pandemics have been reported, all caused by pandemic strains of the O1 serogroup. Vibrio cholerae is a gram-negative bacterium and the causative agent of the diarrhoeal disease cholera.