Cell wall receptor for bacteriophage Mu G(+)

Abstract

The invertible G segment in phage Mu DNA controls the host range of the phage. Depending on the orientation of the G segment, two types of phage particles, G(+) and G(-), are produced which recognize different cell surface receptors. The receptor for Mu G(+) was located in the lipopolysaccharide (LPS) of gram-negative bacteria. The analysis of different LPS core types and of mutants that were made resistant to Mu G(+) shows that the primary receptor site on Escherichia coli K-12 lies in the GlcNAc beta 1 . . . 6Glc alpha 1-2Glc alpha 1-part at the outer end of the LPS. Mu shares this receptor site in E. coli K-12 with the unrelated single-stranded DNA phage St-1. Phage D108, which is related to Mu, and phages P1 and P7, which are unrelated to Mu but contain a homologous invertible DNA segment, have different receptor requirements. Since they also bind to terminal glucose in a different configuration, they adsorb to and infect E. coli K-12 strains with an incomplete LPS core.

High-throughput mapping of the phage resistance landscape inE. coli

“…Despite nearly a century of pioneering molecular work, the mechanistic insights into phage specificity for a given host, infection pathways, and the breadth of bacterial responses to different phages have largely focused on a handful of individual bacterium-phage systems [9][10][11][12][13]. Bacterial sensitivity/resistance to phages is typically characterized using phenotypic methods such as cross-infection patterns against a panel of phages [14][15][16][17][18][19][20][21][22][23][24][25][26][27] or by whole-genome sequencing of phage-resistant mutants [28][29][30][31][32]. As such, our understanding of bacterial resistance mechanisms against phages remains limited, and the field is therefore in need of improved methods to characterize phage-host interactions, determine the generality and diversity of phage resistance mechanisms in nature, and identify the degree of specificity for each bacterial resistance mechanism across diverse phage types [13,25,26,[33][34][35][36][37][38][39][40][41][42][43][44][45][46][47].…”

The cell wall receptor for bacteriophage Mu G(−) inErwiniaandEscherichia coliC

“…Inactivation of the phage by LPS was described previously [8]. LPS was extracted from E. coli C and Erwinia according to the procedure of Galanos [16] and from the other strains by the method of Westphal [17] and purified by ultracentrifugation at 100000 × g. The overall yield of LPS was approx.…”

“…We have shown previously that Mu binds to lipopolysaccharide (LPS) as the cellsurface receptor and furthermore that Mu G(+) and G(-) differ in the recognition of LPS structures [7]. Adsorption of Mu G(+) requires the terminal Glcal,2Glc disaccharide in the cell wall of E. coli K-12 [8]. Interestingly Mu G(+) has somewhat different receptor requirements from phages Pl, P7 and D108 in spite of the fact that these have largely homologous invertible DNA segments and host-range control systems [9].…”

Complex transcriptional and post‐transcriptional regulation of an enzyme for lipopolysaccharide modification

“…Strains carrying a deletion of waaCF (deep rough strains) are resistant to infection with phage P1 (Sandulache et al, 1984). Therefore, in order to transduce the waaCF deletion mutation into the ΔeptB and ΔeptBΔmgrR mutant strain backgrounds, a P1 lysate was prepared on a strain in which the chromosomal ΔwaaCF::tet was complemented by a plasmid.…”