The main tail fibers of xnp1 and xbp1 are mosaic structures with divergent C-terminal regions suggesting they differ in host specificity. Several genes encoding C-terminal tail fiber fragments are present in the same

position in xnp1 and xbp1. Recombination between the main fiber genes and the C-terminal fragments could potentially expand the host range specificity of xenorhabdicin in the respective strains. Bacteria are frequently subjected to infections by bacteriophage that can become resident prophage in the bacterial genome. Prophages can confer fitness advantages, virulence properties, and regions of genomic plasticity to the bacterial host (Asadulghani et al., 2009; Ogier et al., 2010). For instance, the bacteriophage gene pool of enterohemorrhagic Escherichia coli O157:H7 Apoptosis Compound Library cell assay strain Sakai contains many prophage-derived virulence compound screening assay factors (Brussow, 2006). Most of the 24 phage-related elements in E. coli O157:H7 contain genetic modifications and some are now mobile genetic elements capable of dissemination among E. coli strains upon prophage induction (Asadulghani et al., 2009). While the contributions of prophage elements to pathogenicity have been extensively studied, the role of prophage clusters in the

life cycle of mutualistic bacteria remains unclear. Members of the genus Xenorhabdus form mutualistic associations with entomopathogenic nematodes of the genus Steinernema. The bacteria reside in a specialized region of the anterior gut in the infective juvenile form of the nematode (Snyder et al., 2007). The nematode invades soil dwelling insects, migrates through the intestine, and penetrates the midgut to enter the hemocoel, where they release their symbiotic bacteria into the insect blood (hemolymph) to act as insect pathogens (Kaya & Gaugler, 1993; Forst et al., 1997; Goodrich-Blair & Clarke, 2007). Xenorhabdus nematophila provides a nutrient base for nematode reproduction and also produces antimicrobial compounds to suppress the growth of potential competitors (Morales-Soto et al., 2009). Of the 20 known Xenorhabdus species, only two have been sequenced to date; X. nematophila 19061 O-methylated flavonoid and Xenorhabdus bovienii SS-2004,

symbionts of Steinernema carpocapsae and Steinernema jollieti, respectively (Chaston et al., 2011). The ability of X. nematophila to eliminate antagonistic competitors enhances the fitness of its nematode partner (Morales-Soto & Forst, 2011). Xenorhabdus nematophila produces a phage tail-like (R-type) bacteriocin called xenorhabdicin that can kill other Xenorhabdus and Photorhabdus species (Boemare et al., 1992; Sicard et al., 2005; Morales-Soto & Forst, 2011). These proteinaceous structures resemble headless phage tail particles and are composed of conserved tail sheath and tube proteins, as well as several other structural proteins including tail fiber proteins involved in binding to target strains (Boemare et al., 1992; Baghdiguian et al., 1993; Thaler et al., 1995).