Phage Receptor Material in Lactobacillus casei

Abstract

S U M M A R YIn Lactobacillus casei s-I , D-galactosamine and L-rharnnose comprised a phage receptor for phage J-I. A mixture of D-galactosamine and L-rhamnose effectively inactivated phage J-I, and a J-[-resistant mutant strain, L . casei S-I/J-I, lacked D-galactosamine in its surface component. The phage-inactivating effects of D-galactosamine and L-rhamnose were strongly dependent on the concentration of each substance and on temperature.It is suggested that the receptor for phage J-I involves both D-galactosamine in the cytoplasmic membrane and L-rhamnose in the wall of the host bacterium L. casei s-I, which lacks teichoic acid in its wall. I N T R O D U C T I O NIn a previous paper (Yokokura, 1971), it was concluded that L-rhamnose in the wall Lactobacillus casei was one of the components of receptor material for phage J-I since L-rhamnose not only inhibited phage adsorption on to the wall but also desorbed from the wall phages which had been adsorbed to it. The effects of D-galactosamine on these phenomena have been studied. METHODSBacteria and bacteriophage. The bacterial strain, Lactobacillus casei S-I , and the bacteriophage J-I were those previously reported (Yokokura, 197 I). Lactobacillus casei S-I/J-I, which is a mutant strain resistant to phage J-I, was isolated from strain s-I as described by Chatterjee (I 969) using N-methyl-N'-nitro-N-nitrosoguanidine. The Y.P. broth and crude wall, purified wall and TCA (trichloroacetic acid)-soluble fraction were prepared as described previously (Yokokura, 1971). Phage J-I was purified as described by Yamamoto et a/. (1970) using polyethylene glycol. It was inactivated with hexosamine and sugar as follows: a suspension of purified phage J-I [om05 ml, 109 plaque-forming units (p.f.u.) ml-l] was added to 5.0 ml o-I M-Tris/HCl buffer (pH 7.4) containing various hexosamines and sugars, and the mixture was incubated at 37 "C. From this incubation mixture, samples were withdrawn at intervals and the number of active phages was assayed.Chemical analyses. Quantitative analysis for sugars and sugar alcohols in the wall or TCA-soluble fraction was performed as described by Sweeley et al. (1963) with a GC-5A gas-liquid chromatograph (Shimadzu Seisakusho, Kyoto, Japan) equipped with a hydrogen flame ionization detector on a 3 x 1000 mm glass column with 20 % Silicone SE-52 on Celite 545 (Nihon Kuromato Kogyo Co., Tokyo, Japan). Amino acids and hexosamines were estimated with a KLA-3B amino acid autoanalyser (Hitachi, Tokyo, Japan) after hydrolysis as described by Ikawa & Snell (1960). Hexosamines were also estimated by the method of Stewart-Tull (I 968).

Exposing the Secrets of Two Well-Known Lactobacillus casei Phages, J-1 and PL-1, by Genomic and Structural Analysis

“…The uniform distribution of fluorescence suggests the ligands for gp16 binding are not localized in any particular part of the cell but regularly distributed on the cell surface. These observations are consistent with J-1 and PL-1 recognizing saccharide-containing receptors within the outer layer of the cell wall, including a role for L-rhamnose as noted previously (67)(68)(69).…”

Effect of lactic acid bacteria probiotic culture treatment timing onSalmonella Enteritidis in neonatal broilers

“…In experiments 1 to 3, we observed that the PROB culture was significantly more effective at reducing cecal Salmonella Enteritidis than the LAB3 culture. This demonstrates that all lactic acid bacteria are not equally effective at reducing enteric salmonellosis in poultry, as has been described previously (Yokokura, 1997;Kim et al, 2006). Slight differences in surface protein expression between lactobacilli could help describe just one of the possible differences between lactic acid bacteria that effectively prevent enteric infections and those bacteria that confer no protection.…”

Genetic modifications to temperate Enterococcus faecalis phage ϕEf11 that abolish the establishment of lysogeny and sensitivity to repressor, and increase host range and productivity of lytic infection

“…O-acetylation of the lipopolysaccharide side chains, changes in the bonding between the lipopolysaccharide trisaccharide units from a1A4 to b1A4) on the host cell, resulting in the inability of the cell to adsorb additional phage. Although the previous examples of phage receptor modification involve Gram-negative bacteria, it is possible that a similar phenomenon may occur in E. faecalis as the phage receptors in most Gram-positive, low G+C bacteria are cell surface polysaccharides (Vidaver & Brock, 1966;Douglas & Wolin, 1971;Cleary et al, 1977;Yokokura 1977;Keogh & Pettingill, 1983;Valyasevi et al, 1990;Schäfer et al, 1991). If this is the case, then evolutionarily speaking, it may be that originally E. faecalis TUSoD11 was nonlysogenic and possessed cell-surface phage receptors.…”