Structure and function of mutants in the P gene of bacteriophage λ leading to the π phenotype

Reiser, Walter; Leibrecht, Iris; Klein, Albrecht

doi:10.1007/bf00392186

Cited by 8 publications

(5 citation statements)

References 25 publications

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“…The mutation was identified in λ cI 72 mutants that were able to form plaques on the 594 grpD55 host, and is identical to the πA7 mutation previously sequenced [73]. This R137Q single base change partially suppressed P-lethality and fully suppressed plasmid loss at 37-39 ˚C (but not at 42 ˚C where P π was fully expressed) in the dnaB + host.…”

Section: Resultsmentioning

confidence: 77%

Phage Lambda P Protein: Trans-Activation, Inhibition Phenotypes and their Suppression

Hayes

Erker

Horbay

et al. 2013

Viruses

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The initiation of bacteriophage λ replication depends upon interactions between the oriλ DNA site, phage proteins O and P, and E. coli host replication proteins. P exhibits a high affinity for DnaB, the major replicative helicase for unwinding double stranded DNA. The concept of P-lethality relates to the hypothesis that P can sequester DnaB and in turn prevent cellular replication initiation from oriC. Alternatively, it was suggested that P-lethality does not involve an interaction between P and DnaB, but is targeted to DnaA. P-lethality is assessed by examining host cells for transformation by ColE1-type plasmids that can express P, and the absence of transformants is attributed to a lethal effect of P expression. The plasmid we employed enabled conditional expression of P, where under permissive conditions, cells were efficiently transformed. We observed that ColE1 replication and plasmid establishment upon transformation is extremely sensitive to P, and distinguish this effect from P-lethality directed to cells. We show that alleles of dnaB protect the variant cells from P expression. P-dependent cellular filamentation arose in ΔrecA or lexA[Ind-] cells, defective for SOS induction. Replication propagation and restart could represent additional targets for P interference of E. coli replication, beyond the oriC-dependent initiation step.

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Section: Resultsmentioning

confidence: 77%

Phage Lambda P Protein: Trans-Activation, Inhibition Phenotypes and their Suppression

Hayes

Erker

Horbay

et al. 2013

Viruses

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“…The π mutants have been isolated many years ago as phage suppressors of mutations in E. coli dnaB , dnaK , dnaJ and grpE genes [16]. Mutations of the π type have been mapped in the λ P gene [16,17], and more recent biochemical studies demonstrated that a product of one of the π allele ( P ts 1 π A66 ) reveals weaker affinity to DnaB than the wild‐type P protein [18].…”

Section: Discussionmentioning

confidence: 99%

Bacteriophage and host mutants causing the rolling‐circle λ DNA replication early after infection

et al. 2000

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There are two modes of bacteriophage V V DNA replication during its lytic development in Escherichia coli cells. The circle-to-circle (a a) replication predominates at early stages of the phage growth, whereas rolling-circle (c c) replication occurs late after infection to produce long concatemers that serve as substrates for packaging of V V DNA into phage proheads. The mechanism regulating the switch from a a to c c replication remains unknown. Our previous genetic studies indicated that the bacteriophage V V Pts1Z ZA66 mutant cannot replicate at 43³C in the wild-type E. coli host, but it can replicate in the dnaA46(ts) mutant. Density shift experiments suggested that the parental DNA molecules of the infecting phage enter c c replication. Here, using electron microscopy, we demonstrate that as soon as 5 min after infection of the dnaA46(ts) mutant by the V VPts1Z ZA66 phage at 43³C, the c c replication intermediates are highly predominant over a a replication intermediates, contrary to the wild-type conditions (wild-type bacteria infected with the V VP + phage). The initiation of replication of the V VPts1Z ZA66 mutant at 43³C was strongly inhibited in the dnaA + host, as demonstrated by electron microscopy and by pulse-labeling of the phage-derived plasmid replicon. Implications for the mechanism of the regulation of the switch from a a to c c replication mode are discussed.z 2000 Federation of European Biochemical Societies.

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“…Tsurimoto and Matsubara [ 5 ] showed that O protein binds to each ITN as a dimer, thus ori λ should bind four dimers, with higher order binding suggested [ 53 ] to form an O-some that produces torsional stress on the adjacent AT rich region causing the double-stranded DNA to become slightly destabilized and partially unwound [ 54 ]. The N-terminal portion of P was assumed to contain an O-binding domain [ 55 ], while its COOH-terminal domain was suggested to interact with the host DnaB replicative helicase [ 55 , 56 ]. It has been suggested that a complex between O and P is formed that can be independent of DnaB [ 51 , 57 ].…”

Section: Discussionmentioning

confidence: 99%

Complementation Studies of Bacteriophage λ O Amber Mutants by Allelic Forms of O Expressed from Plasmid, and O-P Interaction Phenotypes

2018

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λ genes O and P are required for replication initiation from the bacteriophage λ origin site, oriλ, located within gene O. Questions have persisted for years about whether O-defects can indeed be complemented in trans. We show the effect of original null mutations in O and the influence of four origin mutations (three are in-frame deletions and one is a point mutation) on complementation. This is the first demonstration that O proteins with internal deletions can complement for O activity, and that expression of the N-terminal portion of gene P can completely prevent O complementation. We show that O-P co-expression can limit the lethal effect of P on cell growth. We explore the influence of the contiguous small RNA OOP on O complementation and P-lethality.

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Structure and function of mutants in the P gene of bacteriophage λ leading to the π phenotype

Cited by 8 publications

References 25 publications

Phage Lambda P Protein: Trans-Activation, Inhibition Phenotypes and their Suppression

Phage Lambda P Protein: Trans-Activation, Inhibition Phenotypes and their Suppression

Bacteriophage and host mutants causing the rolling‐circle λ DNA replication early after infection

Complementation Studies of Bacteriophage λ O Amber Mutants by Allelic Forms of O Expressed from Plasmid, and O-P Interaction Phenotypes

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