A P22 bacteriophage mutant defective in antigen conversion

Young, Bobby G.; Fukazawa, Yoshiimura; Hartman, Philip

doi:10.1016/0042-6822(64)90296-x

Cited by 46 publications

(18 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Finally, P22 infection of a host that carries a P22 prophage that is missing its sieA and gtrABC genes (UB-0134) gives normal K + release (figure 4D). This lysogen is defective in superinfection exclusion [45], [46] and O-antigen modification [46], [47] so DNA is injected normally, but the resident P22 prophage repressor is present in the cell and prevents expression of nearly all of the genes of the infecting P22 genome [45], [46]. Thus, expression of the vast majority of P22 genes is not required for K + release.…”

Section: Resultsmentioning

confidence: 99%

The Tip of the Tail Needle Affects the Rate of DNA Delivery by Bacteriophage P22

et al. 2013

View full text Add to dashboard Cite

The P22-like bacteriophages have short tails. Their virions bind to their polysaccharide receptors through six trimeric tailspike proteins that surround the tail tip. These short tails also have a trimeric needle protein that extends beyond the tailspikes from the center of the tail tip, in a position that suggests that it should make first contact with the host’s outer membrane during the infection process. The base of the needle serves as a plug that keeps the DNA in the virion, but role of the needle during adsorption and DNA injection is not well understood. Among the P22-like phages are needle types with two completely different C-terminal distal tip domains. In the phage Sf6-type needle, unlike the other P22-type needle, the distal tip folds into a “knob” with a TNF-like fold, similar to the fiber knobs of bacteriophage PRD1 and Adenovirus. The phage HS1 knob is very similar to that of Sf6, and we report here its crystal structure which, like the Sf6 knob, contains three bound L-glutamate molecules. A chimeric P22 phage with a tail needle that contains the HS1 terminal knob efficiently infects the P22 host, Salmonella enterica, suggesting the knob does not confer host specificity. Likewise, mutations that should abrogate the binding of L-glutamate to the needle do not appear to affect virion function, but several different other genetic changes to the tip of the needle slow down potassium release from the host during infection. These findings suggest that the needle plays a role in phage P22 DNA delivery by controlling the kinetics of DNA ejection into the host.

show abstract

Section: Resultsmentioning

confidence: 99%

The Tip of the Tail Needle Affects the Rate of DNA Delivery by Bacteriophage P22

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Sf6 was isolated and first studied by Gemski et al 14 after it was released from S. flexneri serotype 3a strain [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]. It makes turbid plaques on, and can lysogenize S. flexneri strains of X or Y serotype, for which it is specific.…”

Section: Introductionmentioning

confidence: 99%

The Chromosome of Shigella flexneri Bacteriophage Sf6: Complete Nucleotide Sequence, Genetic Mosaicism, and DNA Packaging

Casjens

Winn-Stapley

Gilcrease

et al. 2004

Journal of Molecular Biology

131

152

View full text Add to dashboard Cite

“…Phage P22 causes attachment of a glucose to C-6 of the galactose of the 0 repeat unit, detectable by appearance of antigen 0 1 ; this antigen is expressed in all or nearly all cells in cultures newly made lysogenic for P22 (Stocker et al, 1960). A mutant phage, P22.a1, does not cause production of factor 1 (Young et al, 1964) because of deficiency of the enzyme for transfer of glucose from antigen carrier lipid to the 0 unit (C. W. Shuster, personal communication; cf. Makela, 1973).…”

Section: (1975)mentioning

confidence: 99%

Lipopolysaccharide Core Defects in Salmonella typhimurium Mutants Which Are Resistant to Felix O Phage but Retain Smooth Character

Hudson¹,

Lindberg²,

Stocker³

1978

Journal of General Microbiology

View full text Add to dashboard Cite

FOR mutants of Salmonella typhimurizrm are resistant to Felix 0 phage, whose receptor includes the N-acetylglucosamine branch of the lipopolysaccharide (LPS) core, but smooth in cultural properties, antigenic character and phage sensitivity pattern (MacPhee et al., 1975). The rfa(F0R) genes determining the FOR character of nine mutants were transduced into a smooth cysEpyrE recipient: the nine FOR transductants (and a tenth FOR mutant) were then made rfb (i.e. unable to make 0 chains) by transduction or Hfr crosses. The rfb FOR strains were sensitive to FO phage but nearly all of them showed a somewhat reduced efficiency of plating and diminished rate of adsorption of the phage. This observation and the Ra (complete core) serological activity of their LPS (tested by haemagglutination inhibition) indicate the presence of some, but less than the normal number of, completed core chains in FOR rfb LPS. On the basis of the sensitivities of the FOR transductants and their rfb derivatives to various ' rough-specific' phages, their increased sensitivities to some antibiotics and to deoxycholate and the serological activity of the rfb FOR LPS in various incomplete core systems, the mutants were divided into three groups: (i) five mutants with probable defects in previously undetected rfa gene(s) concerned with formation of both the galactose I and the galactose 11 units of the LPS core; (ii) two mutants with defects inferred to affect the structure of the inner part of the core and also interfere with addition of the N-acetylglucosamine branch; (iii) three mutants in which no type of incomplete core could be detected, probably affected in formation of the inner part of the core chain. The mutation of one mutant of the last class, unlike those of the other nine mutants tested, lay outside the cysE-pyrE segment, in the 90 to 116 min region of the linkage map. I N T R O D U C T I O NFelix 0 phage (FO phage) attacks nearly all Salmonella with a complete lipopolysaccharide (LPS) core; it acts both on smooth strains, whose LPS core bears 0 chains, and on rough strains which make complete core LPS without 0 chains, i.e. classes rfb and rfaL. F O phage does not attack rough mutants of other rfa classes, which make incomplete LPS core (Wilkinson et al., 1972), nor does it act on galE or galU mutants, which make incomplete core because of their inability to synthesize UDPgalactose or UDPglucose. From its host-range and other evidence it was inferred (for review, see Lindberg, 1973) that the N-acetylglucosamine side branch attached to the distal, glucose 11, unit of the oligosaccharide chain of complete LPS core (Fig. I ) is an essential part of the site of adsorption of FO phage. MacPhee et al. (1975) described a class of Salmonefla fyphimurium mutants, called FOR, which are resistant to FO phage but smooth in cultural and serological

show abstract

A P22 bacteriophage mutant defective in antigen conversion

Cited by 46 publications

References 2 publications

The Tip of the Tail Needle Affects the Rate of DNA Delivery by Bacteriophage P22

The Tip of the Tail Needle Affects the Rate of DNA Delivery by Bacteriophage P22

The Chromosome of Shigella flexneri Bacteriophage Sf6: Complete Nucleotide Sequence, Genetic Mosaicism, and DNA Packaging

Lipopolysaccharide Core Defects in Salmonella typhimurium Mutants Which Are Resistant to Felix O Phage but Retain Smooth Character

Contact Info

Product

Resources

About