Molecular and Genetic Recombination of Bacteriophage T4

Broker, Thomas R.; Doermann, A. H.

doi:10.1146/annurev.ge.09.120175.001241

Cited by 84 publications

(28 citation statements)

References 84 publications

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“…Mutations in genes involved in DNA replication in bacteriophage T4 and in E. coli result in induced recombination (7,37). Many yeast mutants that are known or believed to be deficient in DNA replication also exhibit increased rates of chromosome loss and recombination (21,26).…”

Section: Acaactctcaccacccgcatcccaacgcttpacatctatccaacgeaggacactgaaggtmentioning

confidence: 99%

The phenotype of the minichromosome maintenance mutant mcm3 is characteristic of mutants defective in DNA replication.

Gibson¹,

Surosky²,

Tye³

1990

Mol. Cell. Biol.

132

117

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MCM3 is an essential gene involved in the maintenance of minichromosomes in yeast cells. It encodes a protein of 971 amino acids that shows striking homology to the Mcm2 protein. We have mapped the mcm3-1 mutation on the left arm of chromosome V approximately 3 kb centromere proximal of anpl. The mcm3-1 mutant was found to be thermosensitive for growth. Under permissive growth conditions, it was defective in minichromosome maintenance in an autonomously replicating sequence-specific manner and showed an increase in chromosome loss and recombination. Under nonpermissive conditions, mcm3-1 exhibited a cell cycle arrest phenotype, arresting at the large-bud stage with an undivided nucleus that had a DNA content of nearly 2n. These phenotypes are consistent with incomplete replication of the genome of the mcm3-1 mutant, possibly as a result of limited replication initiation at selective autonomously replicating sequences leading to cell cycle arrest before mitosis. The phenotype exhibited by the mcm3 mutant is very similar to that of mcm2, suggesting that the Mcm2 and Mcm3 proteins may play interacting roles in DNA replication.

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Section: Acaactctcaccacccgcatcccaacgcttpacatctatccaacgeaggacactgaaggtmentioning

confidence: 99%

The phenotype of the minichromosome maintenance mutant mcm3 is characteristic of mutants defective in DNA replication.

Gibson¹,

Surosky²,

Tye³

1990

Mol. Cell. Biol.

132

117

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“…This indicates that recombination and the continuation ofDNA replication are interdependent (for review see ref. 23). The underlying reasons have remained unknown because of observations seemingly inconsistent with simple explanations: the DNA arrest phenotype ofcertain recombinationdefective mutants is overcome by additional mutations in genes 33 and 55 (20)(21)(22)24), which code for RNA polymerase accessory proteins (25)(26)(27).…”

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confidence: 99%

Two alternative mechanisms for initiation of DNA replication forks in bacteriophage T4: priming by RNA polymerase and by recombination.

Luder¹,

Mosig²

1982

Proc. Natl. Acad. Sci. U.S.A.

132

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We show that bacteriophage T4 has two alternative mechanisms to initiate DNA replication: one dependent on Escherichia coli RNA polymerase (RNA nucleotidyltransferase, EC 2.7.7.6), and one dependent on general recombination. Continued DNA synthesis under recombination-defective conditions was sensitive to rifampin, an inhibitor ofRNA polymerase. On the other hand, DNA synthesis accelerated in spite of the presence of rifampin if recombination occurred.Replication ofbacteriophage T4 DNA is initiated on linear DNA molecules at one or several preferred origins (1-9). Soon after the first initiation, many more replication forks are initiated, leading to a rapid acceleration ofDNA synthesis (10, 11). During this acceleration period, a complex network of DNA is formed (12)(13)(14)(15)(16)(17). This process requires recombination functions (9, 18). Most mutations that inhibit recombination not only prevent for, mation of this network but also arrest DNA synthesis prematurely (19)(20)(21)(22). This indicates that recombination and the continuation ofDNA replication are interdependent (for review see ref. 23). The underlying reasons have remained unknown because of observations seemingly inconsistent with simple explanations: the DNA arrest phenotype ofcertain recombinationdefective mutants is overcome by additional mutations in genes 33 and 55 (20-22, 24), which code for RNA polymerase accessory proteins (25)(26)(27).To explain these and other apparently contradictory results, we have proposed that phage T4 uses different modes to initiate DNA replication: initiation from specific origin sequences, which we define as "primary" initiation, and subsequent "secondary" initiation from recombinational intermediates (7,8,28).For several reasons (7,8,29,30) we suspected that host RNA polymerase (RNA nucleotidyltransferase, EC 2.7.7.6) is required for primary initiation although it has been shown that late wild-type DNA replication does not depend on RNA polymerase (31, 32). After the onset of DNA replication, gene 33 and 55 products associate with RNA polymerase (25-27) to effect the switch to late gene expression (33-35) by altering promoter recognition (36). If unmodified host RNA polymerase were required for primary origin initiation, the association with gene 33 and 55 products would shut offreinitiation from primary origins and make the alternative recombinational initiation indispensable for growth of wild-type T4. This hypothesis accounts for the observations mentioned above: premature arrest of DNA synthesis in recombination-defective mutants (46-47-) and restoration of DNA synthesis by additional mutations in genes 33 and 55. Although the rate of DNA synthesis under these conditions is similar to that ofwild-type T4, no branched concatemers are formed (20)(21)(22). Instead, the DNA replicates as linear molecules of unit length, which we suspected to require continued initiation from primary origins by RNA polymerase. Therefore, this replication should remain sensitive to inhibitors of RNA polymerase at late...

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“…There are two ways to form such strands after parental duplexes pair at a region between mutational sites. Since T4 recombination start most frequently by insertion of an exposed single stranded end to the complementary portion of another duplexes (e. g. Broker and Doermann 1975), one pathway may be that such single strand invasions form folks and the displaced single stranded chain are cut and joined by ligation f olloweing repair DNA synthesis to give covalently linked patched or splatched recombinant strands. The other may be that 3'OH end of invading strand is used as a primer to initiate the leading strand DNA replication (Luder and Mosig 1982), and contiguous recombinant strands are formed.…”

Section: Resultsmentioning

confidence: 99%

Genetic analysis of very fast sedimenting DNA of bacteriohage T4.

Miyazaki

Ryo

Minagawa

1985

The Japanese journal of genetics

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We have previously shown that abnormally fast sedimenting DNA which accumulates upon infection of mutants of T4 phage defective in gene 49 is recombination intermediates, while the mutant gives rise to the recombination deficient phenotype, judging from genetic mating tests under the semipermissible condition (Minagawa and Ryo (1979) . To see the step to which the recombination process has proceeded in the DNA, we investigated by the transfection assay whether the generation of contiguous recombinant strands is completed.Such strands were found to be formed normally or nearly normally in the absence of the gene 49 function, supporting the view that the gene product is involved in resolution of branched recombinational intermediates into linear duplexes.

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Molecular and Genetic Recombination of Bacteriophage T4

Cited by 84 publications

References 84 publications

The phenotype of the minichromosome maintenance mutant mcm3 is characteristic of mutants defective in DNA replication.

The phenotype of the minichromosome maintenance mutant mcm3 is characteristic of mutants defective in DNA replication.

Two alternative mechanisms for initiation of DNA replication forks in bacteriophage T4: priming by RNA polymerase and by recombination.

Genetic analysis of very fast sedimenting DNA of bacteriohage T4.

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