Evidence that gene 56 of bacteriophage T4 is a structural gene for deoxycytidine triphosphatase

Munro, Judith L.; Wiberg, John S.

doi:10.1016/0042-6822(68)90169-4

Cited by 16 publications

(8 citation statements)

References 9 publications

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“…It is possible that a host gene product can partially substitute for a missing T4 gene 41 product. Other experiments (unpublished) showed that am mutants of T4 genes 33,39,46,47,52,58,59, 60, and 61 are leaky on strr hosts which completely restricted the growth of am mutants of genes 43, 44 and 62. These observations suggest that many T4 gene products are either partially dispensable or can be substituted for by host gene products.…”

Section: Resultsmentioning

confidence: 98%

Suppression of Amber Mutations of Bacteriophage T4 Gene 43 (DNA Polymerase) by Translational Ambiguity

Karam

O’Donnell

1973

J Virol

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The growth properties of twelve different amber (am) mutants of bacteriophage T4 gene 43 (DNA polymerase) were examined by using nonpermissive (su-) as well as permissive (su+) Escherichia coli hosts. It was found that most of these mutants were measurably suppressed in su-hosts by translational ambiguity (misreading of codons during protein synthesis). The ability of these mutants to grow in response to this form of weak suppression probably means that the T4 gene 43 DNA polymerase can be effective in supporting productive DNA replication when it is supplied in small amounts. By similar criteria, studies with other phage mutants suggested that the products of T4 genes 62 (uncharacterized), 44 (uncharacterized), 42 (dCMP-hydroxymethylase), and 56 (dCTPase) are also effective in small amounts. Some T4 gene products, such as the product of gene 41 (uncharacterized), seem to be partially dispensable for phage growth since am mutants of such genes do propagate, although weakly, in streptomycinresistant su-hosts which appear to have lost the capacity to suppress am mutations by ambiguity.

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Section: Resultsmentioning

confidence: 98%

Suppression of Amber Mutations of Bacteriophage T4 Gene 43 (DNA Polymerase) by Translational Ambiguity

Karam

O’Donnell

1973

J Virol

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“…To construct [das,am] Lacks polynucleotide ligase (12) Lacks DNA-unwinding protein (1) Maturation defective (11) Defective in tail fiber assembly (32) Lacks deoxycytidine monophosphate hydroxymethylase (10,29) DNA arrest (11) DNA arrest (11) DNA arrest (11) DNA arrest (11) DNA arrest (11) DNA arrest (11) Lacks deoxycytidine triphosphatase (21,22) Poor tail fiber attachment (33) DNA arrest suppressor DNA arrest suppressor DNA arrest suppressor DNA arrest suppressor…”

Section: Methodsmentioning

confidence: 99%

“…It seemed possible that the das mutation could represent a change in a phage-coded transfer ribonucleic acid (tRNA) that results in suppression of amber mutants. [A T4 mutation that results in suppression of amber mutations has since been reported (21)]. To test this, several ts mutants in genes 46 and 47 (tsL166X5, tsL86X5, tsA8RX5, and tsAlORX5) were crossed with [das], and the progeny were plated on E. coli B at 42 C. In all cases, plaques were found at a high frequency that were intermediate in size between those formed by [das] alone and those formed by the ts mutants alone.…”

Section: Resutltsmentioning

confidence: 99%

Specific Suppression of Mutations in Genes 46 and 47 by das , a New Class of Mutations in Bacteriophage T4D

Hercules

Wiberg

1971

J Virol

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Mutants in T4 genes 46 and 47 exhibit early cessation of deoxyribonucleic acid (DNA) synthesis ("DNA arrest") and decreased synthesis of late proteins and phage. In addition, mutants in genes 46 and 47 fail to degrade host DNA to acidsoluble products. It is shown here that this complex phenotype can be partially suppressed by mutation of a T4 gene external to genes 46 and 47 which has been named das for "DNA arrest suppressor." The das mutations were discovered as third-site mutations in spontaneous pseudorevertants of [46,47] mutants; the pseudorevertants make small plaques on Escherichia coli B, whereas [46,47] mutants make none. The [das,46,47] triple mutant exhibits increased DNA, late protein, and viable phage production compared to the double mutant [46,47]. The [das,46,47] mutant also degrades more of the host DNA to acid-soluble products than does the [46,47] mutant. The suppressor effect of the das mutation appears to be gene-specific: it suppresses both amber and temperature-sensitive mutations in genes 46 and 47 and does not suppress amber mutations in any of the other genes tested. The [das] single mutants make normal-sized plaques on E. coli B and exhibit nearly normal host DNA degradation, DNA synthesis, late protein synthesis, and viable phage production. The das mutations either define a new gene between genes 33 and 34 or are special mutations within gene 33.

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“…G:C+ A:T transition rates are increased, often strongly; frameshift mutation rates are weakly increased; A : T + G:C transition rates (and perhaps also A:T+ Py:Pu transversion rates) are decreased; and one G: C --f Py: Pu transversion rate is also decreased.These results, together with certain interactions between gene-42 mutator effects and both base analogue mutagenesis and the viral error-prone repair system, suggest that the dHMC hydroxymethylase coded by gene 42 affects mutation rates in a more complex manner than by tho simple regulation of the concentration of the DNA precursor dHMCTP.A striking biochemical oddity of bacteriophage T4 is the complete replacement of cytosine by 5-hydroxymethylcytosine in its DNA (WYATT and COHEN 1953;HERSHEY, DIXON and CHASE 1953). This replacement is brought about as follows: T4 gene 56 encodes a deoxycytidine di-and triphosphatase that rapidly and quantitatively converts dCDP and dCTP to dCMP (WIBERG 1967;MUNRO and WIBERG 1968). Gene 42 encodes a dCMP hydroxymethylase that converts dCMP to 5-hydroxymethyldeoxycytidine monophosphate (dHMCMP) ( FLAKS and COHEN 1959;WIBERG et al 1962).…”

mentioning

confidence: 99%

“…A striking biochemical oddity of bacteriophage T4 is the complete replacement of cytosine by 5-hydroxymethylcytosine in its DNA (WYATT and COHEN 1953;HERSHEY, DIXON and CHASE 1953). This replacement is brought about as follows: T4 gene 56 encodes a deoxycytidine di-and triphosphatase that rapidly and quantitatively converts dCDP and dCTP to dCMP (WIBERG 1967;MUNRO and WIBERG 1968). Gene 42 encodes a dCMP hydroxymethylase that converts dCMP to 5-hydroxymethyldeoxycytidine monophosphate (dHMCMP) ( FLAKS and COHEN 1959;WIBERG et al 1962).…”

mentioning

confidence: 99%

MUTATOR MUTATIONS IN BACTERIOPHAGE T4 GENE 42 (dHMC HYDROXYMETHYLASE)

Williams

Drake

1977

Genetics

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Temperature-sensitive mutations of bacteriophage T4 gene 42 produce diverse effects upon spontaneous mutation rates. G:C → A:T transition rates are increased, often strongly; frameshift mutation rates are weakly increased; A:T → G:C transition rates (and perhaps also A:T → Py:Pu transversion rates) are decreased; and one G:C → Py:Pu transversion rate is also decreased. These results, together with certain interactions between gene-42 mutator effects and both base analogue mutagenesis and the viral error-prone repair system, suggest that the dHMC hydroxymethylase coded by gene 42 affects mutation rates in a more complex manner than by the simple regulation of the concentration of the DNA precursor dHMCTP.

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Evidence that gene 56 of bacteriophage T4 is a structural gene for deoxycytidine triphosphatase

Cited by 16 publications

References 9 publications

Suppression of Amber Mutations of Bacteriophage T4 Gene 43 (DNA Polymerase) by Translational Ambiguity

Suppression of Amber Mutations of Bacteriophage T4 Gene 43 (DNA Polymerase) by Translational Ambiguity

Specific Suppression of Mutations in Genes 46 and 47 by das , a New Class of Mutations in Bacteriophage T4D

MUTATOR MUTATIONS IN BACTERIOPHAGE T4 GENE 42 (dHMC HYDROXYMETHYLASE)

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