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At least 19 recordsLinked to original sources
PubMed1976

The depression of endolysin synthesis in bacteria infected with high multiplicities of phage lambda.

The effect of multiplicity of infection was studied in Escherichia coli with lambda phage, using phage endolysin as an example of a late gene product. A very sensitive endolysin assay method was used so that the initiation time of endolysin synthesis could be more accurately determined. It was observed that high multiplicity of infection (1) increases the rate of lysogenization, (2) progressively delays lysis time, and (3) significantly delays and reduces the synthesis of endolysin in lamdacIII+ cII+ -infected cells. The extent of delay and reduction in endolysin synthesis increases with increasing multiplicity. In contrast, lamdacIII67cII68-infected cells show no delay in endolysin synthesis at high multiplicity of infection when compared with the lamdacIII+ cII+ -infected cells. The results suggest that (1) the expression of cIII and cII genes is multiplicity dependent, (2) high multiplicity of infection enhances the expression of the cIII and cII genes, and (3) the expression of the cIII and cII genes interferes with the expression of the late genes. A model to explain how the expression of the cIII and cII genes interferes with the expression of the late genes is proposed.

Bacteriolysis↗
PubMed1972

Positive control of endolysin synthesis in vitro by the gene N protein of phage lambda.

Positive control in vitro by gene N protein of bacteriophage lambda was demonstrated. lambda DNA was used to direct in vitro synthesis of lambda endolysin in a cell-free protein-synthesizing preparation derived from Escherichia coli. The endolysin synthesis depends on the concomitant in vitro synthesis of lambda gene N protein. When lambda N(-) DNA was used to direct the cell-free preparation, endolysin was made only if extract was added from cells in which a lambda prophage had been induced. The use of various prophage deletion strains proved that if this stimulating activity made in vivo is coded by a known lambda gene, it must be coded by gene N. The ability to stimulate endolysin synthesis in vitro on a lambda N(-) DNA template, therefore, constitutes an assay for N protein.

Chloramphenicol↗
PubMed2026

Integrated computational and experimental benchmarking of Bacillus phage endolysins reveals the relationship between peptidoglycan-fragment recognition descriptors and antibacterial performance.

Protein-based antibacterials such as bacteriophage endolysins offer a targeted therapeutic strategy against Gram-positive pathogens. However, prioritizing the most effective candidates from the large sequence diversity available remains a significant challenge. Here we present a standardized computational-experimental benchmarking framework that evaluates seven phage-derived endolysin variants (E1, E2, E3, E7, E10, E12, and E15) identified from Bacillus genomes. We combined molecular docking and residue-level interaction mapping against muramyl dipeptide (MDP), a minimal conserved peptidoglycan motif, with 1000-ns molecular dynamics simulations, MM/PBSA binding free-energy estimation, and matched functional inhibition assays against Staphylococcus aureus and Micrococcus luteus. Computational analyses revealed generally favorable MDP recognition across variants, albeit with notable differences in contact patterns and complex stability profiles. Experimental screening identified E2 as the most potent antibacterial agent against both species, while E7 and E1 performed strongly in selected computational metrics. Integrated analysis showed only modest correlations between computational descriptors of fragment recognition/stability and observed antibacterial performance. This study establishes a practical comparative benchmarking platform for endolysin candidate prioritization, nominates E2 and E7 as promising candidates for further development, and highlights E1 as a potential structural scaffold for rational engineering, while explicitly demonstrating both the utility and the current limitations of using minimal peptidoglycan fragments as proxies for full cell-wall recognition in lysin benchmarking.

Endopeptidases↗
PubMed1977

Structure and synthesis of a lipid-containing bacteriophage. An endolysin activity associated with bacteriophage PM2.

Endolysin was induced in Pseudomonas BAL-31 infected with bacteriophage PM2 and was also associated with the purified virion. This enzyme required divalent cations for its activity, Ca2+ being the most effective cation. Endolysin activity in the virion increased up to three-fold upon disruption and the activity could be localized in the viral nucleocapsid. Thus the enzyme is localized within the virion. After purification of the structural proteins of bacteriophage PM2, only the nucleocapsid protein (III) had endolysin activity.

Bacteriolysis↗
PubMed1979

Regulation of late functions in Salmonella bacteriophages P22 and L studied by assaying endolysin synthesis.

The rate of endolysin synthesis in Salmonella typhimurium cells infected by bacteriophage P22 or L was taken as a measure for the activity of 23 gene product (the positive regulator for the "late" genes of P22 and L). Endolysin in coded for by gene 19. The amber mutations in gene 23 of P22 and L, used in this study, reduced the rate of endolysin synthesis by a factor of ca. 90 for P22 and of ca. 20 for L. In mixed infections with 19- and 23- mutants the 23 gene products of P22 and L ACT As positive regulators for the respective gene 19 in cis and in trans. Cross-specificity of the 23 gene products, i.e., turning on expression of gene 19 on a chromosome of the other species, could not be demonstrated.

Crosses, Genetic↗
PubMed1990

Cloning, expression and sequence analysis of an endolysin-encoding gene of Lactobacillus bulgaricus bacteriophage mv1.

The lysA gene specifying an endolysin of Lactobacillus delbrueckii subsp. bulgaricus bacteriophage mv1, was cloned and expressed in Escherichia coli. The 4.05-kb restriction fragment containing this gene was analysed by restriction and deletion mapping, and by subcloning. The nucleotide sequence of a 1150-bp fragment coding for an active lysin was determined. The lysA gene consists of 585 bp and codes for a protein of a deduced Mr of 21,120, which agrees with the size based on in vivo transcription/translation studies. The deduced amino acid sequence of the mv1 lysin (LysA) was compared to that of other known lytic enzymes. Significant homology was observed with the N-terminal portion of the muramidase of the fungus Chalaropsis and that of the muramidase of the Streptococcus pneumoniae phage Cp-1, suggesting that LysA might be a muramidase. In E. coli, the cloned lysA gene was able to complement the muramidase-defective bacteriophage lambda Ram5, proving that the products of these two genes are interchangeable. The lysA gene is preceded by an open reading frame with unknown function and no characteristic prokaryotic promoter sequences could be detected upstream from lysA, suggesting that this gene is part of an operon.

Amino Acid Sequence↗
PubMed1967

Lysis inhibition in Escherichia coli infected with bacteriophage T4.

A technique of continuous filtration of T4-infected Escherichia coli has been devised to study the phenomenon of lysis inhibition. Studies using this technique revealed that the length of the lysis delay caused by superinfection can attain only certain discrete values, which for low average multiplicity of superinfection is thought to be a reflection of the actual number of superinfecting particles per cell. The time interval between primary and superinfection had little effect on the length of lysis delay. With increasing rate of superinfection, the length of lysis delay decreased. In superinfected cells, the concentration of endolysin exceeded the final concentration in nonsuperinfected cells. Superinfection of a lysing culture induced lysis inhibition immediately. Temperature-shift experiments, with cells primarily infected by a temperature-sensitive endolysin mutant, revealed that after the normal latent period superinfection was unable to induce lysis inhibition. Amber-restrictive cells, which were primarily infected by an endolysin negative amber mutant, released adenosine triphosphate (ATP) at the end of the normal latent period although lysis did not occur. Superinfection reduced the loss of ATP markedly. The hypothetical role of the cytoplasmic membrane in lysis inhibition is discussed.

Adenosine Triphosphate↗
PubMed1978

Bacteriophage lambda mutants (lambdatp) that overproduce repressor.

Lambda tp mutants, selected for their ability to form turbid plaques on lon hosts, overproduce repressor. The tp1 and tp2 mutations have been located within (or adjacent to) the cIII gene. The tp1 mutation reduced late gene expression, as measured by endolysin synthesis (in the absence of functional cI repressor) and progeny phage yield. The tp4 mutation was mapped in the cY-cII region, and complementation tests indicated that tp4 affects the diffusible product of the cII gene. The tp4 mutation also reduced progeny production, but did not markedly affect endolysin synthesis.

Coliphages↗
PubMed2026

Autoimmune disease-associated pathobionts: mechanisms and therapeutic potential of phage-based approaches.

The gut microbiota is a critical regulator of systemic immune homeostasis; accumulating evidence implicates specific commensal bacteria, termed "pathobionts," in autoimmune disease pathogenesis. However, the definition of pathobionts remains context-dependent, as their effects are influenced by host genetics and host-microbe interactions. In this review, we summarize representative pathobionts supported by functional evidence in selected extraintestinal autoimmune diseases and discuss how these mechanisms may inform phage-based microbiome-targeted interventions. Mechanistically, pathobionts contribute to autoimmune disease through multiple pathways, including molecular mimicry, induction of intestinal T helper 17 and T follicular helper cell responses, disruption of regulatory T cell homeostasis, intestinal barrier dysfunction, and bacterial translocation from the gut to extraintestinal sites. These processes highlight the central role of gut-associated lymphoid tissue in initiating systemic autoimmunity, and targeting disease-associated microbes represents a promising therapeutic strategy. Whole-phage therapy, which enables highly specific bacterial elimination, has shown efficacy in preclinical immune-mediated disease models, but may be affected by variable in vivo replication, bacterial receptor-mediated resistance, anti-phage immune responses, and ecological effects on the resident microbiome. Phage-derived enzymes that lyse bacterial cell walls, such as endolysins, represent a complementary therapeutic modality that specifically targets bacterial peptidoglycan through cell wall-binding and catalytic domains. Collectively, these findings support the concept that pathobiont-targeted interventions, particularly phage-based strategies, may provide microbiome-directed, immunosuppression-sparing therapeutic approaches for selected patient subsets.

Humans↗
PubMed1973

Regulation of the expression of the N gene of bacteriophage lambda.

A quantitative assay for the N protein of bacteriophage lambda has been used to study the in vivo regulation of N gene expression. The assay makes use of the observation that in a cell-free protein-synthesizing system from Escherichia coli programmed with lambdaN(-) DNA the lambda endolysin is made only if N protein is added to the reaction. The rate of synthesis of N protein in vivo is negatively controlled by the products of the CI and tof genes of the phage. Furthermore, N protein activity is extremely unstable in vivo. During normal cell growth at 35 degrees , the half-life of N protein is about 2 min.

Cell-Free System↗
PubMed1975

Recombination-deficient deletions in bacteriophage lambda and their interaction with chi mutations.

We have isolated a new class of deletion mutants of phage lambda that extend from the prophage attachment site, att, into the gam and cIII genes. In this respect they are similar to certain of the lambda pbio transducing phage, but they differ in having a low burst size and in forming minute plaques. Lytically grown stocks of the deletions contain a variable proportion of phage that produce large plaques. These have been shown to carry an additional point mutation. Similar mutations, called chi, have been described by Lam et al. (1974), who showed that they result in a hot-spot for recombination produced by the host recombination system (Rec). We show that chi mutations can occurat several sites in the lambda genome and produce a Rec-dependent increase in the burst size of the one deletion tested.---In addition to reducing burst size, the one deletion tested reduces synthesis of DNA and emdolysin but increases production of serum blocking protein. A chi mutation partially restores DNA synthesis and endolysin production and reduces serum blocking protein to normal levels. Our results are consistent with the hypothesis put forward by Lam et al., that chi enhances the frequency of Rec-promoted recombination, which provides the only pathway for production of maturable DNAin a red gam infection. The mechanism of the differential effect on protein production is, however, unclear.---Chi mutations are found to occur in DNA other than that of lambda. We show that, as has been suggested elsewhere (McMilin, Stahl and Stahy 1974), the lambda pbio transducing phages carry a chi mutation within the E. coli DNA substitution. A chi mutation also arose in a new substitution of unknown origin isolated in the course of this work.

Chromosome Aberrations↗